PREPARED BY

ASHMA SHARMA
 INTRODUCTION
Myocardial infarction is also
known as “Heart Attack”.
Myocardial infarction is the
most common type of
coronary artery disease.
In united states
approximately 1 million
people have myocardial
infarction every year.
DEFINITION
 DEFINITION
Myocardial Infarction is a condition when a
portion of myocardium undergone sustained
ischemia due to inadequate arterial blood
supply causing irreversible cellular death.
TYPES OF MYOCARDIAL
INFARCTION
CORONARY ARTERIES OF
 TYPES OF MYOCARDIUM
INFARCTION
LATERAL WALL M.I. When left circumflex
artery is occluded.

ANTERIOR WALL M.I. When left anterior

descending artery is occluded.

INFERIOR WALL M.I. When right coronary artery

is occluded.
ETIOLOGY??
 ETIOLOGY

NON-MODIFIABLE MODIFIABLE
RISK RISK
FACTORS FACTORS
NON-MODIFIABLE RISK
FACTORS

AGE

FACTOR

FAMILY
HISTORY SEX
AGE: More than 40 years.

FAMILY HISTORY:
Myocardial infarction can be
inherited from parents to
children.

SEX: Myocardial infarction is

3 times more in men than
women.
 MODIFIABLE RISK FACTORS
HIGH
BLOOD
LIPIDS
LEVEL HYPER-
STRESS
TENSION

FACTOR
DIABETES
SMOKING
MELLITUS

PHYSICAL
OBESITY
INACTIVITY
HIGH BLOOD CHOLESTROL LEVEL

LIPIDS
(LIPOPROTIENS)

LOW DENSITY
LIPOPROTEIN HIGH DENSITY
(LDL) LIPOPROTEIN
DANGEROUS (HDL)
HDL is not dangerous because it contains
more proteins & very less lipids.
Secondly it carry lipids away from arteries
to the liver for metabolism. So it prevents
lipids accumulation within arteries.
LDL is dangerous because it contains more
lipids & has capacity to deposit fat within
arteries.
So, LDL level more than 160mg/dl will
place a person at a risk of myocardial
infarction.
 HYPERTENSION

If a person’s blood pressure is more than

140/90 mmHg continuously for 4-5 years
Sustained stress on arterial walls injury
to endothelial lining atherosclerosis
narrowed & thickened arterial walls
risk of M.I.
Also salt consumption 5gms/ day cause M.I.
 SMOKING
Smoking nicotine catecholamine (epinephrine &
nor epinephrine) release increases heart rate &
blood pressure increases cardiac workload.
+
CO decreases O2 available to myocardium

Injury to myocardium
PHYSICAL INACTIVITY

Improper lipid metabolism

LDL level increases

Starts accumulating
in blood vessels

Risk of M.I.
 OBESITY

More lipids are produced

LDL level increases

Atherosclerosis

Risk of M.I.
 DIABETES MELLITUS

Glucose molecules may be stick to

lumen of artery

Blockage of artery

Risk of having M.I.

 STRESS
SNS stimulation

Release of catecholamine

Increases heart rate & intensify the force of

myocardial contraction

Increases O2 demand

Cell death

Risk of M.I.
PATHOPHYSIOLOGY
 Causative factor: Obesity

Atherosclerosis

Narrowing of lumen

ed heart insufficient blood flow to myocardium

Contractility ed O2 demand of myocardial cells

Inadequate creates an O2 deficit

Blood supply
myocardial cell death inflammation
Oliguria
CK-MB & Troponine released Fever
 Anaerobic glycolysis

Accumulation of lactic acid

Irritation of myocardial nerve fibers

Transmission of pain massage to myocardium

Chest pain & radiation towards shoulder & arm

Stimulation of vomiting SNS Stimulation
center
increased
Nausea & Vomiting catecholamine

Diaphoresis Increased
(perfuse sweating) Heart Rate

Cold & Clammy skin

“Cold Sweat”
 CLINICAL
MANIFESTATIONS
 PAIN
Characteristics: Severe,
immobilizing chest pain.
Usually prescribed as
heaviness, pressure, tightness,
burning.
Location: Substernal,
Retrosternal or Epigestric.
Radiation: It may radiate to
neck, jaw, arm or back.
Duration: Lasts for 20 minutes
or more.
 NAUSEA & VOMITING
Stimulation of vomiting center by severe
pain causes nausea & vomiting.

FEVER
100.4 to 102.2 F
It is due to inflammatory process caused by
Myocardial cell death.
 SYMPATHETIC NERVOUS
SYSTEM STIMULATION

Increased catecholamine releases.

Diaphoresis (perfuse sweating).

Cold & clammy skin (“cold sweat”).

 CARDIOVASCULAR
MANIFESTATIONS
Hypotension

Decrease cardiac output

Shock

Urine output (Oliguria): <30ml/day.

Dyspnoea
DIAGNOSTIC TESTS
 ECG
During M.I., the classic ECG changes are:
T-wave inversion, ST-segment elevation &
development of abnormal Q-wave.
SERUM CARDIAC MARKERS

TROPONINE-T
CK-MB (ENZYME)
(PROTEIN)

HEMATOLOGICAL TEST: Increase in

SGOT, LDL level, WBC (12000-14000/mm3)
count.
 ECHOCARDIOGRAM
PURPOSE: It is done to evaluate ventricular
function by checking ejection rate.
MEGNATIC RESONANCE IMAGING (MRI)
PURPOSE: To detect damage to myocardial
cells.
 ANGIOGRAPHY

To detect percentage of blockage & type of

mi.
CHEST X-RAY
To detect cardiomegaly.
MANAGEMENT
MEDICAL MANAGEMENT

MEDICAL
MANAGEMENT

DRUG
FIBRINOLYTIC
THERAPY
THERAPY
 DRUG THERAPY
ANALGESIC: Morphine Sulphate.
NITRATES
I/V Nitroglycerine: 4 ampules of NTG are dissolved in
100 ml normal saline to reduce pain by dilating
coronary arteries.
Sublingual Nitroglycerine: (Sorbitrate)
At one time patient can take 3 tablets.
if pain relieved If pain not relieved

Take second Tab. After 10 take next Tab. at same time

minutes
BETA ADRENERGIC BLOCKERS
(Propanolol) it inhibit SNS stimulation of heart.
Thus reduces both heart rate & contractility

CALCIUM CHANNEL BLOCKERS

(Verapamil, Nifedipine)
It causes coronary artery vasodilatation & decreases
myocardial contractility.
Increases blood supply to myocardium & decreases
O2 demand of myocardium.

LOW-MOLECULAR-WEIGHT HEPARIN
(Fragmine)
These inhibit conversion of fibrinogen into fibrin.
 FIBRINOLYTIC THERAPY
TIME OF
ADMINISTRATION:
Thrombolytics are given to the
patient within 24 hours of onset
of chest pain
ACTION: These will dissolve &
do lysis of thrombus in
coronary artery.
DOSE: Streptokinase (2
Ampules) are given in 500ml
normal saline.
 INDICATIONS
Chest pain for >20 minutes, unrelieved by
nitroglycerine.
CONTRAINDICATIONS
Active bleeding
Known bleeding disorder
Recent major surgery
NURSING CONSIDERATION

All invasive procedures should be done

before giving fibrinolytic therapy.
Minimize the number of pricks on patient’s
skin.
Avoid I/M injection.
Treat minor bleeding by pressing punctured
area.
SURGICAL MANAGEMENT
PTCA (Percutaneous
Transluminal
Coronary
Angioplasty)
STENT PLACEMENT
 ATHERECTOMY
With Atherectomy the plaque is shaved off
using a type of rotational blade.
CORONARY ARTERY BYPASS
GRAFT (CABG)
A portion of saphenous vein from leg is
removed & is anastmosed proximally to the
ascending aorta & distally to coronary
artery.
NURSING MANAGEMENT
 NURSING ASSESSMENT
SUBJECTIVE DATA:
Past history of M.I., Angina, hypertension.
Medication: use of nitrates, calcium channel
blockers, antihypertensive drugs.
Chest pain: squeezing, sharp & radiation to
jaw, neck, arm.
OBJECTIVE DATA:
General: anxiety, diaphoresis.
Integumentary: cool, clammy skin.
Cardiovascular signs & findings
 NURSING DIAGNOSIS
Acute pain related to myocardial ischemia
& decreased myocardial oxygen supply as
manifested by severe chest pain & radiation
of pain to neck & arms.

Ineffective cardiopulmonary tissue

perfusion related to reduced coronary blood
flow as manifested by decrease in B.P.,
Dyspnea, peripheral oedema & oliguria.
Ineffective gas exchange related to fluid
overload as manifested by crackles in chest
due to pulmonary oedema.
Anxiety related to threat of death, pain &
changes in health status as manifested by
restlessness, agitation.
Knowledge deficit related to disease
process, medication, home activities &
rehabilitation as manifested by frequent
questioning about illness & management.
 COMPLICATIONS

CONGESTIVE
ARRYTHMIAS HEART CARIOGENIC
FAILURE SHOCK
SUMMERIZATION
RECAPTUALIZATION
 ASSIGNMENT
You have to write an assignment on “Dietary
Plan for patient with Myocardial Infarction”
& submit it on 30-7-2009.
 BIBLIOGRAPHY
LEWIS, HEITKEMPER, DIRKSEN; MEDICAL
SURGICAL NURSING, SIXTH EDITION, MOSBY,
NEW YORK. 2004. PAGE 802-830
SMELTZER SUZANNE C., MEDICAL SURGICAL
NURSING, TENTH EDITION, LIPPINCOTT
WILLIAMS & WILKINS, NEW YORK. 2004. PAGE
725-735.
BLACK JOYCE M., HAWKS JANE HOKANSON,
MEDICAL SURGICAL NURSING, SEVENTH
EDITION, VOLUME SECOND, ELSEVIER
PUBLISHERS, NEW DELHI. 2005. PAGE 1707-1730.