Acute Myocardial Infarction

Sarah Priore RN BSN

 Objectives
– Define and understand the epidemiology of
MI’s and how they are classified
– Will be able to identify the risk factors
associated with MI’s
– Will be able to recognize signs and symptoms
of acute MI and what the appropriate
interventions are.
– Understand the treatment options available to
treat acute MI.
 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.
• MI’s are described by the area of
occurrence.
• Anterior, Inferior, Lateral or Posterior.
Coronary Artery Anatomy
 Coronary artery events
• Ischemia – Outer most area, source of
arrhythmias, viable if no further infarction.
• Injury – Viable tissue found between
ischemic and infarcted areas.
• Infarction/necrosis – Center area, dead
not viable tissue that turn into scar.
 MI Classifications
• MI’s can be subcategorized by anatomy
and clinical diagnostic information.
Anatomic
• Transmural and Subendocardial
Diagnostic
• ST elevations (STEMI) and non ST
elevations (NSTEMI).
 Epidemiology
• MI’s are the leading cause of death in the
United States, affecting one in five men
and one in six women.
• 450,000 people in the US die from
coronary disease each year.
• Incidence rates increase with age as do
mortality rates due to infarction.
 Epidemiology
• The survival rate for those hospitalized
due to MI has reached approximately
95%.
• This is the result of the advancements
made in modern medical technology.
 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, LDL’s or
triglycerides are associated with the
increased risk of coronary plaque
formation and MI.
• Almost 50% of the U.S.
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.
 Pathophysiology
• Ischemia develops when there is an
increased demand for oxygen or a
decreased supply of oxygen.
• Ischemia can develop within 10 seconds
and if it lasts longer than 20 minutes,
irreversible cell and tissue death occurs.
• Myocardial cell death begins at the
endocardium. The area most distal to the
arterial blood supply.
 Pathophysiology
• As vessel occlusion continues cell death
spreads to the myocardium and eventually
to the epicardium.
• Severity of the MI depends on three
factors.
– Level of occlusion
– Length of time of occlusion
– Presence or absence of collateral circulation
 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.
 Video
• Watch your own heart attack…This is a
little graphic!

http://www.youtube.com/watch?v=LUt1xXASm_
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 EKG’s should be taken to rule
out or confirm MI.
• 12 lead EKG’s can help to distinguish
between ST-elevation MI’s and Non-ST-
elevation MI’s.
Normal Sinus Rhythm
 Angina
Stable
• Chest pain caused by the build up of lactic
acid and irritation to the myocardial nerve
fibers.
• Chest pain caused by the 4 E’s.
• Pain is usually relieved with rest, pain
meds and nitrates.
 Variable/Prinzmetal/Spasm
• Transient ischemia that occurs
unpredictably and almost always at rest.
• Pain is caused by vasospasm of the
arteries.
• ST segment elevations will be noted.
 Unstable
• Chest pain at rest or with exercise and
tends to last greater than 15 minutes.
• This results in reversible myocardial
ischemia but is a sign that an infarct is
soon to come.
• EKG will reveal ST segment depression
and T wave inversion.
 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
 Phases of a STEMI
• Hyperacute Phase
– Occurs within the first few hours of MI onset.
– Leads facing the infarcted surface: ST
segment elevation.
– Leads facing the uninjured surface: ST
segment depression (reciprocals)
– T waves become tall, widened and might be
taller than the R wave.
 Phases of a STEMI
• Fully Evolved Phase
– Q wave development
– ST elevation
– T waves start to become inverted in leads
facing the injury.
 Phases of a STEMI
• Resolution phase
– Weeks after there will be a gradual return of
ST segments to baseline.
– T waves will gradually return to normal but are
the last to change back.
 Serum 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.
Serum Cardiac Markers
 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 MI’s.
• 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.
 Cardiac Catheterization
• Upon arrival to the cath lab all actue MI
patients will receive:
– A bolus dose of plavix
– IV Integrelin
– Heparin dose either subcu or IV drip
– Angiomax : a DTI may be substituted for
heparin and integrelin.
 Cardiac Catheterization while
undergoing an MI
• http://www.youtube.com/watch?v=TS0Je1m9Q

Angioplasty and Stenting

http://www.youtube.com/watch?v=9FPapBbbS4
 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.
 References
• Bolooki, H.M.& Askari, A. (Published August 8 2010).
Acute Myocardial Infarction. Retrieved from
http://www.clevelandclinicmeded.com/medicalpubs/disea
semanagement/cardiology/acute-myocardial-
infarction/#s0050
• Lewis, S., Heitkemper, M., & Dirksen, S. (2004). Medical
surgical nursing assessment and management of clinical
problems. St. Louis, MO: Mosby.
• McCance, K.L., Huether, S.E., Brashers, V.L.& Rote,
N.S. (2010). Pathophysiology the biological basis for
disease in adults and children. Maryland Heights, MO:
Mosby Elsevier.