S.NO.

SPECIFIC CONTENT MATTER TEACHING LEARNING EVALUATION

OBJECTIVE ACTIVITIES
1. INTRODUCTION
The heart muscle must have
adequate blood supply to
contract properly. The
coronary arteries carry
oxygen to 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 MYOCARDIAL INFARCTION The student teacher defines What do you mean
Myocardial Myocardial infarction is leading cause of MI verbally. by Myocardial
infarction. sudden death in men and women. It is caused infarction?
by an obstruction in a coronary artery
resulting in necrosis to the tissues supplied by
the artery. The obstruction is usually due
atherosclerotic plaque, a thrombus or an
embolism. The area most affected is left
ventricle.
What are the
3. Enlist the risk The student teacher
RISK FACTORS various risk
factors of enumerates the risk factors
factors of MI.
Myocardial of MI on PPT.
NON-MODIFIABLE RISK FACTORS:-
infarction. -Family history
-Increasing age
-Race
 -Male gender

MODIFIABLE RISK FACTORS:-

-Blood lipid level abnormalities
-Diabetes mellitus
-Hypertension
-Physical inactivity
-Obesity
-Cigarette smoking
-Alcohol consumption

4. Describe the PATHOPHYSIOLOGY The student teacher explains What are the
pathophysiology pathophysiology by using pathophysiological
of MI in detail. In an MI, an area of myocardium is ppt. Changes occurring
permanently destroyed. MI is usually caused in MI?
by reduced blood flow in a coronary artery
due to rupture of atherosclerotic plaque and
subsequent occlusion of artery by the
thrombus. Other causes of MI are vasospasm
of coronary artery, decreased 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.

5. Enumerate the CLINICAL MANIFESTATIONS What are the

clinical Cardiovascular The student teacher clinical
manifestations of -Chest pain or discomfort, palpitations. enumerates the clinical manifestations of
MI -Increased blood pressure. manifestations by using ppt. MI?
-pulse deficit
 -ST segment and T wave changes.
Respiratory
-Shortness of breath
-Dyspnea,tachypnea
-crackles
-pulmonary edema
Gastrointestinal
-nausea and vomiting
Genitourinary
-Decreased urinary output indicates
cardiogenic shock.
Skin
-cool,clammy ,diaphoretic and pale
appearance due to sympathetic stimulation
may indicate cardiogenic shock
Neurologic
-Anxiety,restlessness,light headedeness
Psychological
-Fear with feeling of impending doom.

6. Discuss the ASSESSMENT AND DIAGNOSTIC FINDINGS The student teacher What are the
assessment and The diagnosis of MI is based on the presenting discusses the diagnostic diagnostics
diagnostic symptoms and laboratory test results.The techniques with the help of measures used to
findings of MI prognosis depends on the severity of coronary ppt and lecture cum diagnose MI?
artery obstruction and extent of myocardial discussion
damage. Physical examination is always
conducted.but the examination alone does not
confirm the diagnosis.
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
include the risk factors for heart disease.
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
nondiagnoctic.The echocardiogram can detect
hypokinetic and akinetic wall motion and can
determine the ejection fraction.
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 oncrease 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 I
and T are specific for cardiac muscles and
these tests are currently recognised 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.

7. Enlist the COMPLICATIONS The student teacher enlists What are the
complications of  Acute pulmonary edema the complications with the complications of
MI  Heart failure help of chart MI?
 Cardiogenic shock
 Dysrhythmias
 Pericardial effusion
 Myocardial rupture

8. Explain the MEDICAL/SURGICAL MANAGEMENT The student teacher What can be the
medical It focuses on reducing the workload of describes the medical medical
management of heart,relieving pain,improving tissue management with the help management of
the patient with perfusion,preventing complications and of ppt. the patient with
MI. further tissue damage.Immediately after MI a MI?
client is admitted to a coronary unit.The client
heart is contantly 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
aspirin,nitroglycerin,morphine,beta blockers
and other medications as indicated.Patients
should receive beta blockers
initially,throughout the hospitalisation and
after discharge.These medications decrease
the incidence of future cardiac events.
Thrombolytics:-
These medications are administered I/V , can
be given directly into coronary artery in
cardiac catheterization lab. The purpose of
thrombolytics is to dissolve and luse the
thrombus in a coronary artery,causing
reperfusion and minimize the size of
infarction.
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 relax
the bronchioles to enhance the
oxygenation.The cardiovascular response to
morphine is monitored closely,particularly B.P
which can decrease and repiratory rate can be
depressed.
ACE inhibitors:-
ACE inhibitors prevent the conversion of
angiotensin I to angiotensin II.In the absence
of angiotensin II B.P will decrease and kidneys
excrete sodium and fluid which further
decreases the oxygen demand of the heart.
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 amiodrone. Ventricular
tachycardias is treated with lidocaine or
cardioversion.If the dysrhythmias are
continous then magnesium sulphate can be
given.
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:-
-Supplemental oxygen
-Nitroglycerin
-Morphine
-Aspirin 162-325mg
-Beta blockers
-Angiotensin converting enzyme inhibitors
within 24 hours.
→Evaluate for indications for reperfusion
therapy:-
-Percutaneous coronary intervention
-Thrombolytic therapy
→Continue therapy as indicated:-
-I/V heparin/low molecular weight heparin
-Clopidogrel or ticlopidine
-Glycoprotein IIb/IIIa inhibitor
-Bed rest(12-24 hours)

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.Supirior outcomes
have been reported with the use of PCI
compared to thrombolytics.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.
 NURSING MANAGEMENT The student teacher What will the
Elaborate the elaborates the nursing nursing care of the
nursing The nursing priorities are management with the help patient with MI?
management of of ppt.
the patient with 1) To relieve pain, anxiety.
MI in detail
2)To reduce myocardial workload.'

3)To prevent and assist in treatment of life

threatening disarrythmias.

4) To promote self care.

NURSING DIAGNOSIS, INTERVENTION AND

RATIONALE

I. 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.

Intervention: .Instruct patient to report pain

immediately.

Rationale: Delay in reporting pain hinders pain

relief.

Intervention: Provide calm and quiet

environment and other comfort measures.

Rationale: Decreased external stimuli may

aggravate anxiety.

Intervention: Administer supplementary

oxygen.

Rationale: Increases the oxygen supply to

myocardium thereby relieving discomfort.

II. Anxiety / fear related to change in health

and socio economic status manifested by
apprehension, increased tension, restlessness,
uncertainty etc.

Interventions: Note presence of hostility

withdrawal or denial.

Rationale: Ongoing anxiety may be 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.
III. Altered tissue perfusion related to
reduction of blood flow due to vaso
constriction manifested by thrombo embolitic
formation.

Interventions: Inspect for cyanosis, cold and

clammy skin.

Rationale: Systemic vasoconstriction resulting

from decreased cardiac output may be
evidenced by decreased skin perfusion.

Intervention: Assess for homan's sign,

erythema and edema.

Rationale: Indicator for deep vein thrombosis.

Interventions: Monitor laboratory details eg:

ABG' S BUN Indicators of organ perfusion.
Prepare the patient for thromboembolytic
therapy.

Rationale: To dissolve the clot and to restore

perfusion of myocardium.

IV. Excess fluid volume related to increased

sodium and water retention manifested by
dependent edema.

Interventions: Measure intake output to detect

whether there is decrease in output.

Rationale: Decreased cardiac output results in

impaired kidney perfusion. Na/H2o retention
and reduced urine output.

Intervention: Weigh daily

Rationale: Sudden changes in weight indicate

fluid imbalance.

Intervention: Provide low sodium diet.

Rationale: Sodium will enhance fluid retention.

Intervention: Note the development of

dependent edema.

Rationale: Indicates development of CHF.

Intervention: Administer diuretics as

prescribed.

Rationale: To correct fluid overload.

V. Knowledge deficit related to lack of factual

information regarding implications of heart
disease and future health status manifested by
anxiety, worries, gloomy face etc.

Interventions: Assess patient's level -of

knowledge and ability to learn.

Rationale: It is necessary to create individual

instruction plan.

Intervention: Educate the patient about basic

informations regarding M.I., its cause,
prevention and management.

Rationale: Patient will gain adequate

knowledge about his disease and will try to
avoid a second attack.

Intervention: Emphasize on the importance of

avoiding the risk factors of M.I.

Rationale: Modifiable risk factors can be

prevented if we take adequate precautions.

OTHER NURSING MANAGEMENT:

Provide semi-fowler's positions to promote

chest expansions and comfort. Oxygen
administration to treat tissue hypoxia. Check
vital signs every 15 minutes. Watch for PVC
(Premature Ventricular Contractions) in the
ECG. Assess the L.O.C. Morphine is the drug of
choice to relieve chest pain. Strict I/O chart.
Bed rest. Sedation and hypnotics to relieve
unnecessary anxiety. Clear liquid diet for 48
hours and thereafter soft bland diet. Cardiac
enzymes should be repeated. Educate the
patient to control diet high in fats and
cholesterol.
Summary:
Today we have dealt with:
 Definition of MI
 Risk factors
 Pathophysiology
 Clinical manifestations
  Diagnostic findings
 Medical management
 Nursing management

Conclusion :

MI is a life threatening
disease caused by many
factors. Health education
must be given to the
patients with predisposing
or risk factors to prevent it.
Early diagnosis is also very
important for saving the life
of the patient.

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