Acute Myocardial

Infarction
Prepared by:
Dr Rajesh T Eapen
ATLAS HOSPITAL
MUSCAT

Definition
Otherwise know as heart attack
An MI occurs when there is a diminished
blood supply to the heart which leads to
myocardial cell damage and ischemia.
Contractile function stops in the necrotic
areas of the heart.
Ischemia usually occurs due to blockage
of the coronary vessels.

Definition cont.
This blockage is often the result of
thrombus that is superimposed on an
ulcerated or unstable atherosclerotic
plaque formation in the coronary artery.
MIs are described by the area of
occurrence.
Anterior, Inferior, Lateral or Posterior.

Coronary Artery Anatomy

MI Classifications
MIs can be subcategorized by anatomy
and clinical diagnostic information.
Anatomic
Transmural and Subendocardial
Diagnostic
ST elevations (STEMI) and non ST
elevations (NSTEMI).

Risk Factors
The presence of any risk factor is
associated with doubling the risk of an MI.
Non Modifiable
Age
Gender
Family history

Risk Factors
Modifiable

Smoking
Diabetes Control
Hypertension
Hyperlipidemia
Obesity
Physical Inactivity

Smoking
Tobacco use increases the risk of
coronary artery disease two to six times
more than non smokers.
Nicotine increases platelet thrombus
adhesion and vessel inflammation.

Diabetes & Hypertension

Diabetes not only increases the rate of
atherosclerotic formation in vascular
vessels but also at an earlier age.
The constant stress of high blood
pressure has been associated with the
increased rate of plaque formation.
Shearing Stress and inflammation of
endothelial lining begins the process.

Hyperlipidemia
Elevated levels of cholesterol, LDLs or
triglycerides are associated with the
increased risk of coronary plaque
formation and MI.
Almost 50% of the
population has some
form of dyslipidemia.

Obesity and Physical Inactivity

Mortality rate from CAD is higher in those
who are obese.
Some evidence shows that those who
carry their weight in their abdomen have a
higher incidence of CAD
Physically inactive people have lower HDL
levels with higher LDL levels and an
increase in clot formation.

Signs and Symptoms

Signs and symptoms are unique to each
individual patient.
Ranging from no symptoms to sudden
cardiac arrest.

Chest Pain
The most common initial manifestation is
chest pain or discomfort.
This is not relieved by rest, position
change or nitrate administration.
Pain is described by heaviness, pressure,
fullness and crushing sensation.
Not everyone experiences this sensation.

Chest Pain
PQRST assessment for chest
pain
P- Precipitating events
Q- Quality of pain
R- Radiation of pain
S- Severity of pain
T- Timing

Nausea and Vomiting

Not everyone will experience this.
Vomiting results as a reflex from severe
pain.
Vasovagal reflexes initiated from area of
ischemia.

Sympathetic Nervous System

Stimulation

During an MI increased catecholamines

are released.
This results in diaphoresis and
vasoconstriction of peripheral blood
vessels.
Cool Sweat with a temperature increase
during the first 24 hours.

Cardiovascular Changes
Initially the BP and pulse may be elevated.
Later, BP will drop due to decreased
cardiac output.
Urine output will decrease
Lung sounds will change to crackles
Jugular veins may become distended and
have obvious pulsations.

Within the first 10 minutes upon

arrival to the hospital:
Check vital signs and evaluate oxygen
saturation
Establish IV access
Obtain and review 12-lead ECG
Take a brief focused history and perform a
physical exam
Obtain blood samples to evaluate initial cardiac
markers, electrolytes and coagulation

Diagnostics
After collecting patient health history, a
series of ECGs should be taken to rule
out or confirm MI.
12 lead ECG can help to distinguish
between ST-elevation MIs and Non-STelevation MIs.

Normal Sinus Rhythm

STEMI

ST segment elevations
T wave changes
Q wave development
Enzyme elevations
Reciprocals

NSTEMI
ST segment
depressions
T wave changes
No Q wave
development
Mild enzyme elevations
No reciprocals

STEMI vs. NSTEMI

InvestigationSerum Cardiac Markers

Myocardial cells produce certain proteins
and enzymes associated with cellular
functions.
When cell death occurs, these cellular
enzymes are released into the blood
stream.
CPK and troponin

CPK

Creatine Phosphokinase
Begin to rise 3 to 12 hours after acute MI.
Peak in 24 hours
Return to normal in 2 to 3 days

Troponin
Myocardial muscle protein released into
circulation after injury.
These are highly specific indicators of MI.
Troponin rises quickly like CK but will
continue to stay elevated for 2 weeks.
Myoglobin-lacks cardiac specificity.

Treatment Options
The immediate goal for any acute MI is to
restore normal coronary blood flow to
vessels and salvage myocardium.
There are a variety of medical and
medicinal therapies to treat an MI.

General Treatment for the MI

patient
MONA

Morphine
Oxygen
Nitroglycerin
Aspirin

Fibrinolytic Therapy
Indicated for patients with STEMI MIs.
Should be given within 12 hours of
symptom onset.
Fibrinolytics will break down clots found
within the vessles
Contraindications: post op surgical
patients, history of hemorrhagic stroke,
ulcer disease, pregnancy, ect.

Cardiac Catheterization
A diagnostic angiography which includes
angioplasty and possible stenting.
Performed by an interventional
cardiologist with a cardiac surgeon on
stand by.
Percutaneous procedure through the
femoral or brachial artery.

Coronary artery bypass graft

Surgical treatment where saphenous vein
is harvested from the lower leg and used
to bypass the occluded vessels.

Long Term Care

Smoking Cessation and lifestyle
modifications.
Aspirin, Beta Blockers and Clopidogrel will
be indefinite.
Lipid lowering medication along with diet
modifications.

Myocardial infarction
Nursing process
Assessment

A careful history
Description of symptoms (chest pain,
palpitation, dyspnea, syncope or
sweating). Each symptom must be
evaluated with regard to time, duration,
precipitating & relieving factors. In
addition complete physical assessment
for:
level of consciousness

Nursing process (cont)

*Heart sounds
*Peripheral pulses
*Lung sound

Nursing process (cont)

Nursing diagnosis
Chest pain related to reduced coronary blood
flow.
High risk for breathing pattern ineffective related
to fluid overload
Anxiety related to fear from death
High risk for tissue perfusion alteration related to
decreased cardiac output
Health maintenance alteration related to no
adherence to therapeutic regimen

Nursing Management of MI
Nursing interventions for a patient with acute MI
focus on:
Achieving a balance between myocardial oxygen
supply and demand: This means that in the acute
phase, there is a need to increase myocardial oxygen
supply by oxygen administration to prevent tissue
hypoxia. Myocardial oxygen supply can be enhanced
by the administration of coronary artery vasodilators
(nitroglycerin).
Prevention of complications: Nurses need to apply
cardiac monitoring of patient to detect early
ventricular dysrhythmias. In addition, nurses should
continue to assess for signs of ischemic pain.

Nursing Management of MI (Continued)

Health education: Nurses should focus on:
Pathophysiology of acute MI.
Description of signs and symptoms such as pain.
pressure, or heaviness in chest.
Notification of nurses of any changes in chest pain
intensity.
Avoidance of the Valsalva maneuver.
Risk factors modification, including:

Daily fat intake < 30% of total calories.

Maintain serum cholesterol level < 200 mg/dL.
Maintain LDL cholesterol to < 70 mg/dL.
Stop smoking and reduce daily salt intake.
Control hypertension and diabetes mellitus.
Increase physical activity and reduce weight

Nursing Management of MI (Continued)

Health education (Continued): Nurses should focus
on:
Medication teaching: indications and side effects.
Follow-up care after discharge.

THANK YOU