MYOCARDIAL

INFARCTION
PRESENTED BYSANDEEP KAUR

INTRODUCTION
Myocardial infarction (MI)

refers to the process by which

areas of myocardial cells in the
heart are permanently destroyed.
It occurs when myocardial

tissues are abruptly and

severely deprived of oxygen.

DEFINITION
Myocardial infarction is a

diseased condition which is

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

CORONARY ARTERIES OF HEART

LOCATION / TYPES OF MYPCARDIAL INFARCTION

Obstruction of the left anterior descending artery

(LAD) results in anterior or septal wall MI.

Contd..
Obstruction of the circumflex artery results in

posterior wall MI or lateral wall MI.

Obstruction of the right coronary artery results in
inferior wall MI.

ETIOLOGY

ETIOLOGY

NON-MODIFIABLE
RISK
FACTORS

MODIFIABLE
RISK
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.
GENDER: Myocardial
infarction is 3 times more in
men than women.

MODIFIABLE RISK FACTORS

HIGH BLOOD CHOLESTROL LEVEL

LIPIDS
(LIPOPROTIENS)

LOW DENSITY
LIPOPROTEIN
(LDL)
DANGEROUS

HIGH DENSITY
LIPOPROTEIN
(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 persons 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 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
Contractility

insufficient blood flow to myocardium

ed O2 demand of myocardial cells

Inadequate
Blood supply

creates an O2 deficit
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
center
Nausea & Vomiting

Diaphoresis
(perfuse sweating)
Cold & Clammy skin
Cold Sweat

SNS Stimulation
increased
catecholamine

Increased
Heart Rate

CLINICAL MANIFESTATIONS
Cardiovascular Chest pain/Discomfort
Palpitations
Elevated BP
ECG may show tachycardia, bradycardia and

dysarrythmia

CONTD..
Respiratory Shortness of breath
Dyspnea/Tachypnea
Crackles
Pulmonary edema-may be present

Gastrointestinal Nausea
Vomiting

CONTD..
Genitourinary Decreased urinary output

Skin Cool, clammy skin

Diaphoresis
Pallor, Cyanosis
Coolness of extremities

CONTD..
Neurogenic Anxiety, restleness
Light- headedness
Headache
Visual Disturbances
Altered speech
Altered motor functions
Altered level of consciousness

CONTD..
Psychosocial Fear feeling
Pt. may deny that anything is wrong

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 102.2F
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

ASSESSMENT/DIAGNOSTIC
FINDINGS
It is generally based on presenting symptoms,

ECG and laboratory test results.

Patient history-it includes
Description of presenting

symptoms
History of previous illness,

family health history

CONTD..
Electrocardiogram-

ECG provides information that

assists in diagnosing acute MI.
The classic ECG changes are T wave inversion
ST segment elevation
Abnormal Q wave

CONTD..

Contd..

SERUM CARDIAC MARKERS

CK-MB (ENZYME)

TROPONINE-T
(PROTEIN)

CK-MB- increases 3-6 hrs after onset of chest

pain, peaks in 12-18 hrs & return to normal

within 3-4 days.
Cardiac troponin T- increases 7-14 hrs after MI

& persists for 5-7 days.

LDH- it increases 14-24 hrs after onset of MI,

peak within 48-72 hrs & slowly return to

normal over next 7-14 days.
AST- it increases within several hrs after onset

of pain, peaks within 12-18 hrs & return to

normal within 3-4 days.
Leukocytosis- (10,000-20,000/mm3 ) appears

on second day after MI & diappears in 1 wk.

ECHOCARDIOGRAM
PURPOSE: it is useful to assess the ability of
heart muscles to contract & relax.
It is done to evaluate ventricular function by checking
ejection rate.
MEGNATIC RESONANCE IMAGING (MRI)
PURPOSE: To detect site & extent of myocardial cells.

ANGIOGRAPHY
To detect percentage of blockage & type of MI.

CHEST X-RAY
To detect cardiomegaly.

Positron emission tomography- (PET scan)

It is used to evaluate cardiac metabolism & to

assess tissue perfusion.

MEDICAL MANAGEMENT
MEDICAL
MANAGEMENT

DRUG
THERAPY

FIBRINOLYTIC
THERAPY

MEDICAL MANAGEMENT
The goal of medical management is to minimize

myocardial damage, preserve myocardial function

and prevent complications.
Pharmacological management Thrombolytics
Analgesics
ACE Inhibitors(ACE-I)

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
minutes

take next Tab. at same time

BETA ADRENERGIC BLOCKERS

(Propanolol) it inhibit SNS stimulation of heart.
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 upto 12 hours of onset of
chest pain but for best results it
should be given within 1 hr
after onset of chest pain.
ACTION: These will dissolve &
do lysis of thrombus in
coronary artery.
It includes streoptokinase,
urokinase, t-PA, alteplase.
After thrombolytic therapy, IV
heparin is continued.

Absolute & relative

contraindications for
thrombolytic therapy
Absolute contraindicationsAny prior ICH
Ischemic stroke within 3 months
Known structural cerebral vascular lesion
Known malignant intracranial neoplasm
Active bleeding or bleeding dissection
Significant closed head trauma within past

3 months

Relative contraindicationsHistory of chronic, severe, poorly controlled

hypertension
Severe uncontrolled hypertension on
presentation
History of prior ischemic stroke >3months
Dementia
Pregnancy
Active peptic ulcer
Current use of anticoagulants, the higher the
INR the greater the risk
Allergic reaction to streptokinase or
antistreplase

Pts. with NSTEMI is diagnosed with elevation

of cardiac markers.
They are not candidates for immediate
thrombolytic therapy but should receive antiischemic therapy.
If STEMI is present, the goal is to achieve a

door- to drug time of 30 min & a door-to

balloon time of within 90 min.

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.

COMPLICATIONS
Dysrrythmias
Cardiogenic shock
Heart failure
Pulmonary embolism
Recurrent MI
Dresslers syndrome

NURSING MANAGEMENT

Nursing assessmnetSUBJECTIVE 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 interventions in acute stage Obtain a description of chest discomfort

Assess vital signs
Assess cardiovascular status
Place client in semi-fowlers position
Administer oxygen
Establish I/V access
Administer NTG as prescribed

CONTD..
Administer Morphine Sulfate as prescribed.
Obtain 12-lead ECG
Administer I/V and anti-dysrrythmics as prescribed
Monitor thrombolytic therapy
Monitor for signs of bleeding
Monitor lab values
Assess distal peripheral pulses

CONTD..
Monitor intake-output
Assess resp. rate and breath sounds
Provide reassurance to client and family

CONTD..
Interventions following acute stage Maintain bed rest for 24-36 hrs.
Provide range of motion exercises
Monitor for complications
Encourage client to verbalize feelings regarding

MI

Nursing diagnosis
Acute pain R/T myocardial ischemia resulting from

coronary artery occlusion

Outcome- the client will experience improved
comfort as evidenced by dec. in pain rating scale.
Interventions- assess characteristics of pain
Assess respiration, BP, heart rate with each episode
of chest pain.
Obtain 12 lead WCG on admission & on each episode
of chest pain.
Monitor respond to drug therapy.
Limit visitors.
As morphine as ordered.
Administer nitrates as ordered.

Ineffective tissue perfusion R/T thrombus in

coronary artery
Outcome- the client will demonstrate
improved cardiac tissue perfusion as
evidenced by dec. rating of pain.
Interventions- provide bed rest.
Administer oxygen as prescribed.
Administer thrombolytics.
Monitor ST segments.

Dysrrhythmias R/T electrical instability or

irritability secondary to infarcted tissue

Outcome- the client will have no dysrrythmias
as evidenced by normal sinus rhythm.
Interventions- teach client & family about need
for continous monitoring.
Assess apical heart rate.
Give antidysrrythmic agents as ordered.
Monitor effects of antidysrrythmics.
Monitor serum K levels.
Maintain patent IV line.
Monitor ST segments & document changes.

Decreased cardiac output R/T negativ einotropic

changes in heart secondary to myocardial ischemia.

Outcome- the client will have improved cardiac output
as evidenced by normal cardiac rate, rhythm &
hemodynamic parameters.
Interventions- assess mental status of pt.
Assess lung sounds for crackles & ronchi.
Monitor BP .
Assess heart sounds for murmur.
Monitor urine output.
Assess for peripheral perfusion-cyanosis, peripheral
pulses.
Monitor ABG.
Maintain hemodynamic stability & duration.

Impaired gas exchange R/T decreased cardiac

output.
Outcome- the client will demonstrate
improved gas exchange as evidenced by
absence of dyspnea.
Interventions- administer oxygen as ordered.
Monitor ABG.
Continue to assess clients skin, capillary refill
& level of consciousness.
Assess respiratory status for dyspnea &
crackles.
Prepare for intubation & mechanical
ventilation if hypoxia inc.

Risk for bleeding R/T coagulopathies with

thrombolytic therapy.
Powerlessness R/T a near-death experience &
anticipated lifestyle changes.
Anxiety & fear R/T hospital admission & fear
of death.
Risk for constipation R/T bed rest, pain
medications & NPO or soft diet.
Ineffective health maintenance R/T MI &
implications for lifestyle changes.
Risk for activity intolerance R/T an imbalance
b/w oxygen supply & demand.

Risk for heart failure R/T disease progress as

evidenced by tachycardia, hypotension or

hypertension.
Excess fluid volume R/T reduced GFR,
decreased cardiac output, increased ADH
hormone & sodium & water retention.
Risk for impaired skin integrity R/T bed rest &
decreased tissue perfusion.

THANKS

THANK
S