myocardial infarction,symptoms,diagnosis,classification,treatment and comlications

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.