Acute myocardial infarction, or heart attack, occurs when blood supply to the heart is diminished leading to cell damage and death. It is usually caused by a blockage in the coronary arteries from atherosclerotic plaque or a blood clot. Diagnosis involves EKGs, blood tests of cardiac enzymes, and imaging tests. Treatment depends on the type and severity of MI but may include medications to break up clots, angioplasty and stenting, or coronary bypass surgery. Complications can affect the heart muscles and blood vessels if not properly treated.

1. Acute MyocArdiAl infArction
by
RAMKUMAR

2. 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.

3. 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.

4. Coronary Artery Anatomy

5. 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.

8. 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).

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

10. Risk Factors
Modifiable
• Smoking
• Diabetes Control
• Hypertension
• Hyperlipidemia
• Obesity
• Physical Inactivity

11. 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.

12. 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

13. Symptoms:
• Pain is the cardinal symptom of an
MI
• Anxiety and fear of impending
death
• Nausea and vomiting
• Breathlessness
• Collapse/syncope

14. 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.

15. 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.

16. DIAGNOSTICS:
• Electrocardiogram (ECG)
• Blood test (Cardiac enzymes)
• Echocardiogram
• Nuclear scan
• Chest radiographs
• Coronary angiography
• Exercise stress test.
• Cardiac computerized tomography (CT)
or magnetic resonance imaging (MRI).

17. 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.

18. Normal Sinus Rhythm

19. 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.

20. 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.

21. 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.

22. STEMI
• ST segment elevations
• T wave changes
• Q wave development
• Enzyme elevations
• Reciprocals

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

24. STEMI vs. NSTEMI

25. 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.

26. Phases of a STEMI
• Fully Evolved Phase
• Q wave development
• ST elevation
• T waves start to become inverted in
leads facing the injury.

27. 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.

28. 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

29. 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

30. 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.

31. 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.

32. General Treatment for the MI
patient
• Morphine
• Oxygen
• Nitroglycerin
• Aspirin

33. 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.

34. 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.

35. 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.

36. Coronary artery bypass graft
• Surgical treatment where saphenous vein
is harvested from the lower leg and used
to bypass the occluded vessels.

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

39. Complications
Vascular Complications
• Recurrent ischemia
• Recurrent infarction
Mechanical Complications
• Left ventricular free wall rupture
• Ventricular septal rupture
• Papillary muscle rupture with
acute mitral regurgitation

40. COMPLICATION:
Myocardial Complications
• Diastolic dysfunction
• Systolic dysfunction
• Congestive heart failure
• Hypotension/cardiogenic shock
• Right ventricular infarction
• Ventricular cavity dilation
• Aneurysm formation (true, false)

41. 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.