Myocardial

Infarction
ERICKA JANE S. BARRIOS,
R.N.

INTRODUCTION
ACUTE MYOCARDIAL INFARCTION (AMI or
MI) commonly known as a HEART
ATTACK, is a disease state that when
the blood supply to the part of the heart
is interrupted, results in ISCHEMIA or
OXYGEN SHORTAGE leads to damage
and potential death of heart tissue.
The term MYOCARDIAL INFARCTION is
derived from MYOCARDIUM (heart
muscle) and INFARCTION (tissue death
due to oxygen starvation)

DEFINITION
MI may be defined as a process by
which the blood supply to the
myocardial cells is interrupted due to
occlusion of a coronary artery by
atherosclerotic plaque, embolus or
thrombus, leads to ischemia of these
cells and if it continued for a prolonged
period then it causes permanent injury
to the cells (myocardium), ultimately
leads to INFARCTION and is not able to
meet
the
metabolic
needs
of
the
cells.
MYOCARDIAL
INFARCTION
is
IRREVERSIBLE PROCESS.

CORONARY ARTERIES OF THE

HEART

ETIOLOGY
NON-MODIFIABLE
RISK FACTORS

MODIFIABLE RISK
FACTORS

Increasing Age
Family History

Hyperlipidemia

Gender

Smoking

Hypertension
Physical Inactivity
Obesity
Diabetes Mellitus
Stress

NON-MODIFIABLE RISK
FACTORS
AGE: more than 40 years old.

FAMILY HISTORY: MI can be inherited from

parents to children.

GENDER: MI is 3 times more in men

than women.

MODIFIABLE
RISK FACTORS

Hyperlipidemia
LIPIDS
(LIPOPROTEI
NS)

LOW
DENSITY
LIPOPROTEI
N (LDL)

DANGERO
US

HIGH
DENSITY
LIPOPROTEI
N (HDL)

LDL is dangerous because it contains more lipids and has capacity

to deposit fat within the arteries.
So, LDL level more than 160mg/dl will place a person at a risk of MI.

Hypertension
BLOOD PRESSURE is more than 140/90
mmHg continuously for 4-5 years
Sustained stress on arterial walls
Injury to endothelial lining
ATHEROSCLEROSIS

RISK OF MI

Also salt consumption 5 gms/day

Smoking
Nicotine releases catecholamine
(epinephrine & norepinephrine)
Increases heart rate
& blood pressure
increases cardiac
load

CO decreases O2
availability to
myocardium

INJURY TO
MYOCARDIUM

Physical Inactivity
Improper lipid metabolism
LDL Level increases
Starts accumulating in blood vessels

RISK FOR MI

Obesity
More lipids are produced
LDL level increases
ATHEROSCLEROSIS

RISK FOR MI

Diabetes Mellitus
Glucose molecules may stick to lumen of
artey
Blockage of artery

Risk of having MI

Stress
SNS
Stimulation
Release of
catecholamine
Increase heart rate & intensify the
force of myocardial contraction
Increases O2
demand
Cell death

Risk of MI

PATHOPHYSIOLO
GY

Predisposing Factors
Premature, Accelerated Atherosclerosis
Progressive narrowing of
blood vessels

Risk for excessive blood clot

formation

Ischemia of the heart

muscle

Thromboembolism
Hypoxia
Necrosis

Aerobic to
unaerobic
metabolism
Lactic acid
formation
Chest pain/
Muscle spasm

Release of
lysozomal
enzyme
Altered
depolarization
Altered
repolarization
MYOCARDIA
L

Decreased
myocardial
contractility
Decreased cardiac
output
Renal ischemia/
Oliguria

MI almost always occur in the left ventricle due to

occlusion of left anterior descending artery
(LADA) and often significantly depresses left
ventricular function (anterior wall infarction)
Alteration in function depend on size and location
of an infarct.
Contractile function in the
necrotic area cease
permanently.
Healing requires
formation of scar tissues
that replace the necrotic
myocardial muscle.
Scar tissue inhibits
contractility.

CLASSIFICATION OF
MI
TRANSMURAL INFARCT
extends from endocardium to epicardium
SUBENDOCARDIAL INFARCT
affects the endocardial muscles
INTRAMURAL INFARCT
seen in patchy areas of the myocardium;
equally associated with angina pectoris

3 AREAS WHICH DEVELOP

IN MI
ZONE OF INFARCT
records pathologic Q wave in the ECG
ZONE OF INJURY
gives rise to elevated ST segment
ZONE OF ISCHEMIA
produces inversion of T wave

COMPLICATIONS OF
DYSRHYTHMIAS MI
CARDIOGENIC SHOCK
PERICARDITIS
RUPTURE OF MYOCARDIUM
VENTRICULAR ANEURYSM
CHRONIC HEART FAILURE (CHF)

ASSESSMENT
FINDINGS

PAIN
Cardinal symptom of MI: persistent,
crushing substernal pain that may
radiate to the left arm, jaw, neck, and
shoulder blades.
Unreleived by rest or nitroglycerine

ANXIETY &
APPREHENSION
Feeling of doom, restlessness

SHOC
Systolic pressure <80mmHg, lethargy,
K

cold clammy skin, diaphoresis,

peripheral cyanosis, tachy/bradycardia,
weak pulse

OLIGURIA
Urine flow <30mL/hr

FEVER
Slight temperature elevation within
24hour & extends 3-7days with
leukocytosis, elevated ESR

INDEGISTION
gas pains around the heart, nausea &
vomiting

ACUTE PULMONARY
Sense of suffocation, dyspnea,
EDEMA
orthopnea, gurggling, bubbling
respiration

MEDICAL
MANAGEMENT

IMMEDIATE ASSESSMENT

Elevation of bed
Loosen tight clothing around neck
Measure vital signs
Measure oxygen saturation
Obtain IV access
12 lead ECG
Perform brief history
Obtain initial serum cardiac
markers level

ANALGESIC
Relief of pain
This is a priority because pain may
cause
shock IV Morphine sulfate, lidocaine
Administer
or Nitroglycerine

THROMBOLYTIC THERAPY
Disintegrate blood clot by activating
fibrinolytic processes
Streptokinase, Urokinase, Tissue
pladminogen Activator (TPA)
Administration is most crucial between 36h after initial infarction has occurred

 Detect for occult bleeding during & after

thrombolytic therapy
Assess neurologic status changes (may
indicate GI bleeding or cardiac
tamponade)
ANTICOAGULANT AND ANTIPLATELET
MEDICATIONS
Administered after thrombolytic therapy
to maintain arterial patency.

DIAGNOSTIC
EVALUATION

Electrocardiogram (ECG)
It provides information that assists in
diagnosing acute MI.

The classic ECG changes are:

T wave inversion
ST segment elevation
Abnormal Q wave

Blood test (Cardiac

Enzymes)
Cardiac enzymes are released from the
heart into the blood stream during
myocardial damage.
It can be used in the diagnosis of an MI.
1. TOTAL CREATINE KINASE
LEVEL
Rises within 3h after the onset of
chest pain
Peaks within 24h after damage and
death of cardiac tissue
2. CK-MB Isoenzyme
Peak elevation: 18-24h after onset of
chest pain

3. TROPONIN LEVEL
Rises within 3h
Remains elevated up to 3 weeks
4. MYOGLOBIN
Rises within 1h after cell death
Peaks in 6h
Returns to normal within 24-36h or
less
5. LDH Level
Rises 24h after MI
Peaks 48-72h
Falls to normal in 7days
6. WBC
Elevated WBC (10,000-20,000
cells/mm3 ) on 2nd day following MI

Echocardiogram
It is useful to assess the ability of heart
muscles to contract and relax.
It is done to evaluate ventricular function
by checking ejection rate.

Cardiac Computerized
Tomography (CT) or Magnetic
Resonance
Imaging
(MRI)

To detect site and extend of myocardial

cells.

Angiography
To detect
percentage
blockage & type
of MI.
It remains the
most accurate in
diagnosing the
percentage of
blockage in
coronary arteries.

Chest X-ray
To detect cardiomegaly

Exercise Tolerance Test or

Stress
Test

Assess for electrocardiographic changes

and ischemia
Evaluate for
medical therapy
Identify
patients who
may need
invasive
therapy

Thallium or Nuclear Scan

Assess ischemia or necrotic muscle tisue.

NURSING
MANAGEMENT

1NURSING DIAGNOSIS:

ACUTE PAIN R/T MYOCARDIAL ISCHEMIA

RESULTING FROM CORONARY ARTERY
OCCLUSION, AN IMBALANCE BETWEEN
MYOCARDIAL OXYGEN SUPPLY & DEMAND.

GOAL:
TO REDUCE OR ELIMINATE CHEST
DISCOMFORT.

INTERVENTIONS:
1. ASSESS PATIENTS DESCRIPTION OF CHEST
DISCOMFORT.
2. ASSESS BLOOD PRESSURE, HEART RATE &
RHYTHM, AND RESPIRATORY RATE.
3. ASSESS THE SKIN FOR TEMPERATURE AND
MOISTNESS.
4. OBTAIN A 12-LEAD ECG DURING CHEST
DISCOMFORT.
5. ADMINISTER OXYGEN, NTG, IV MORPHINE, OR
OTHER MEDICATION AS ORDERED.
6. PROVIDE A RESTFUL ENVIRONMENT: BY
ELEVATING HEAD OF BED.
7. PROVIDE CARE IN CALM, QUIET
ENVIRONMENT.

2NURSING DIAGNOSIS:

INEFFECTIVE TISSUE PERFUSION RELATED TO

AN IMBALANCE BETWEEN MYOCARDIAL
OXYGEN SUPPLY & DEMAND AND
MANIFESTED BY CHEST DISCOMFORT,
DYSRHYTHMIAS.

GOAL:
TO REDUCE OR ELIMINATE MANIFESTATIONS
OF DECREASED MYOCARDIAL TISSUE
PERFUSSION.

INTERVENTIONS:
1. KEEP THE PATIENT ON BED REST WITH A
QUIET ENVIRONMENT.
2. ADMINISTER OXYGEN AND ANTIRRHYTHMIC
AND OTHER MEDICATIONS AS ORDERED AND
CONTINUOUSLY EVALUATING PATIENT
CONDITION.
3. ADMINISTER THROMBOLYTICS OR SEND THE
PATIENT FOR ANGIOPLASTY AS ORDERED.
4. MONITOR ST SEGMENTS.

3NURSING DIAGNOSIS:

DECREASED SYSTEMIC TISSUE PERFUSSION

RELATED TO A DECREASE IN CARDIAC
OUTPUT FROM ARRHYTHMIAS AND
CONDUCTIVE DISTURBANCES.

GOAL:
1. TO REDUCE OR ELIMINATE MANIFESTATIONS
OF DECREASED SYSTEMIC TISSUE
PERFUSION.
2. PREVENT MANIFESTATIONS OF DECREASED
SYSTEMIC TISSUE PERFUSION.

INTERVENTIONS:
1. DECREASED PATIENT PHYSICAL ACTIVITY.
2. ADMINISTER OXYGEN AND ANTIRRHYTHMIC
AND OTHER MEDICATIONS.
3. ASSESS FOR PERIPHERAL PERFUSION: BY
MONITORING SKIN FOR CYANOSIS, PALLOR,
COOLNESS, DIAPHORESIS AND PERIPHERAL
PULSES.
4. CHECK FOR CEREBRAL PERFUSION: BY
CHECKING MENTAL STATUS (RESTLESSNESS,
DECREASED RESPONSIVENESS)

5. AUSCULTATE FOR LUNG SOUNDS:

BY MONITORING FOR CRACKLES.
6. AUSCULTATE FOR HEART SOUNDS:
NOTE THE PRESENCE OF GALLOP,
MURMUR, AND INCREASED OR DECREASED
HEART RATE.
7. CHECK FOR RENAL PERFUSION:
DECREASED URINE OUTPUT.
8. MONITOR ARTERIAL BLOOD GAS LEVELS.

4NURSING DIAGNOSIS:

IMPAIRED GAS EXCHANGE RELATED TO

DECREASED CARDIAC OUTPUT AS
EVIDENCED BY CYANOSIS, IMPAIRED
CAPILLIARY REFILL TIME AND DYSPNEA.

GOAL:
TO IMPROVE GAS EXCHANGE.

INTERVENTIONS:
1. ADMINISTER OXYGEN AS ORDERED.
2. MAINTAIN ABGs AS ORDERED.
3. CONTINUE TO ASSESS THE PATIENTS SKIN,
CAPILLIARY REFILL, AND LEVEL OF
CONSCIOUSNESS EVERY 2 TO 4 HOURS.
4. ASSESS RESPIRATORY STATUS FOR DYSPNEA
AND CRACKLES.
5. PREPARE FOR INTUBATION & MECHANICAL
VENTILATION IF HYPOXIA INCREASES.

5NURSING DIAGNOSIS:

ANXIETY AND FEAR RELATED TO DIAGNOSIS,

TREATMENT, AND PROGNOSIS OF ANGINA
MANIFESTED BY ABNORMAL RATE AND
RHYTHM OF PULSE AND RESPIRATION,
ELEVATED BLOOD PRESSURE.

GOAL:
TO ALLAY ANXIETY AND FEAR.

INTERVENTIONS:
1. ASSESS AND DOCUMENT THE PATIENTS AND
FAMILYS LEVEL OF FEAR AND ANXIETY AND
EFFECTIVENESS OF COPING MECHANISM.
2. PROVIDE CONTINUITY OF CARE.
3. ALLOW AND ENCOURAGE THE PATIENT AND
FAMILY TO ASK QUESTIONS.
4. ALLOW THE PATIENT AND FAMILY TO
VERBALIZE FEARS.
5. PROVIDE A COMFORTABLE, QUIET
ENVIRONMENT FOR THE PATIENT AND FAMILY.

6NURSING DIAGNOSIS:

KNOWLEDGE DEFICIT RELATED TO

MYOCARDIAL INFARCTION, TREATMENT,
PROGNOSIS, AND RISK FACTORS.

GOAL:
TO GIVE ADEQUATE KNOWLEDGE ABOUT HIS
DISEASE PROCESS.

INTERVENTIONS:
1. DEVELOPMENT OFA TEACHING PLAN
ENABLES THE NURSE TO PROMOTE
STANDARDIZED CONTENT TO EACH PATIENT.
2. TEACH PATIENT TO DECREASE PHYSICAL
ACTIVITY AND TAKE NTG AS PRESCRIBED
DURING PERIODS OF ANGINA.
3. TEACH PATIENT TO SEEK MEDICAL
ATTENTION IMMEDIATELY IF RELIEF OF CHEST
PAIN HAS NOT OCCURRED WITHIN 30mins.

4. PROVIDE A CONCRETE INFORMATION ABOUT

DIAGNOSTIC PROCEDURES PERFORMED ON
PATIENT AND THE RATIONALE BEHIND IT.
5. TEACH PATIENT & RELATIVES ABOUT THE
IMPORTANCE OF CHANGING LIFESTYLE.
PROVIDE INFORMATION ABOUT
MODIFICATION OF RISK FACTORS.
6. TEACH PATIENT TO REDUCE PRECIPITATING
FACTORS.

THE
END