This document defines myocardial infarction and describes its causes, symptoms, diagnosis, and treatment. A myocardial infarction occurs when blood flow to the heart is blocked, causing heart cell death. It causes chest pain and other symptoms like nausea and shortness of breath. Diagnosis involves EKGs, blood tests of cardiac enzymes, and cardiac catheterization. Treatment depends on the severity but may include clot-busting drugs, angioplasty, stents, or coronary bypass surgery to restore blood flow. Goals are to preserve heart function and prevent complications like arrhythmias or heart failure.

1. MYOCARDIAL INFARCTION

2. Definition
• Acute myocardial infarction (MI) is a clinical
syndrome that results from occlusion of a
coronary artery, with resultant death of cardiac
myocytes in the region supplied by that artery.
Defined by “Current diagnosis and treatment in Cardiology - 2013”

4. • The degree of altered function depends on the
area of heart involved and the size of infarction
• In acute MI cardiac cells can withstand
ischemic conditions for approximately 20
minutes before cellular death begins
• It takes 4-6 hours for the entire thickness of
the heart to become necrosed

5. CLASSIFICATION

6. CLASSIFICATION
• AWMI
• IWMI
• PWMI
• LWMI
• RVMI

7. ETIOLOGY AND PATHOPHYSIOLOGY

8. CLINICAL MANIFESTATIONS
CHEST PAIN

9. SYMPATHETIC NERVOUS SYSTEM
STIMULATION
• CATECHOLAMINE RELEASE
• DIAPHORESIS
• COOL AND CLAMMY EXTRIMITIES DUE TO
VASOCONSTRICTION

10. CARDIOVASCULAR
MANIFESTATIONS
• TACHYCARDIA
• ELEVATED BP INITIALLY
• CRACKLES ON AUSCULTATION

11. • NAUSEA
• VOMITING AS A RESULT OF VASOVAGAL
REFLEX BY SEVERE PAIN
• FEVER- 100.4 F AS A RESULT OF INFLAMATION

12. Diagnostics
• History collection, physical exmn
• 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.

13. NORMAL SINUS RHYTHM

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

15. 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.

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

19. STEMI vs. NSTEMI

20. 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

21. 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

22. 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.

23. • Cardiac catheterization
• echocardiography

24. COMPLICATIONS
• DYSRHYTHMIAS
Most common present 80% patients
• HEART FAILURE
occur when the pumping power of heart
diminished
• CARDIOGENIC SHOCK
Inadequate oxygen and nutrients are
supplied to the tissues because of severe LV
dysfunction

25. • PAPILLARY MUSCLE DYSFUNCTION
valvular dysfuction, causes- MR,TR
• VENTRICULAR ANEURYSM
Myocardial wall thinned and bulges out
during contraction
• PERICARDITIS
• DRESSLER SYNDROME
pericarditis with effusion and fever develops
4-6 weeks after MI

26. MANAGEMENT
• preserve cardiac muscle fibers
• Vital signs
• Iv assess
• ECG
• Biomarkers

27. MANAGEMENT
• INITIAL MANAGEMENT
M- Morphine
O- oxygen
N-Nitrates
A- Antiplatelets

28. EMERGENT PERCUTANEOUS CORONARY
INTERVENTION (PCI)
• PCI may be used to open the occluded
coronary artery in an acute MI and promote
reperfusion to the area that has been deprived
of oxygen.
• PCI is performed should be less than 90
minutes.

29. • Usually PCI with the placement of stent will be
performed
• Complications- dissection of ccoronary artery
• Cardiac tamponade
• Restenosis
• Hematoma formation at the site

30. Thrombolytic therapy/fibrinolytic
therapy
• The purpose of thrombolytics is to dissolve and
lyse the thrombus in a coronary artery
(thrombolysis), allowing blood to flow through the
coronary artery again (reperfusion), minimizing the
size of the infarction, and preserving ventricular
function

31. Indications
• Chest pain for longer than 20 minutes,
unrelieved by nitroglycerin
• ST-segment elevation in at least two leads that
face the same area of the heart
• Less than 24 hours from onset of pain

32. Absolute Contraindications
• Active bleeding
• Known bleeding disorder
• History of hemorrhagic stroke
• History of intracranial vessel malformation
• Recent major surgery or trauma

33. Relative contraindications
• Active peptic ulcer disease
• Pregnancy
• Stroke more than 3 months back
• Uncontrolled hypertension

34. • Start within 30 minutes( door-to-needle time)

35. Common thrombolytics
1st generation
• Streptokinase
• Urokinase
2nd generation
• alteplase ( tPA)
• reteplase
• Anistreplase

36. Nursing considerations
• Minimize the number of times the patient’s skin is
punctured.
• Avoid intramuscular injections.
• Draw blood for laboratory tests when starting the
IV line.
• Monitor for acute dysrhythmias, hypotension, and
allergic reaction.
• Monitor for reperfusion: resolution of angina or
acute ST-segment changes.
• Check for signs and symptoms of bleeding:

37. Pharmacologic management
• Analgesics
morphine sulphate
decreases preload and afterload
reduce anxitey
• Nitrates
IV nitroglycerin

38. • ACE inhibitors
increases the left ventricular function
prevent ventricular remodelling
• Beta-adrenergic blockers
decreases the contractility and myocardial
oxygen demand
• Cholesterol lowering agents
• Stool softeners

39. SURGICAL MANAGEMENT
• CORONARY ARTERY BYPASS GRAFT(CABG)
Construction of new conduits between aorta
or other major arteries with help of CPB machine
Indications
Triple vessel disease
60% occlusion of LAD
Fails medical management

40. Grafts used
Internal mammary artery
Great saphenous vein
Inferior epigastric artery
Radial artery

41. Nursing Management
• Assessment
subjective data
objective data

42. Diagnosis
• Ineffective cardiopulmonary tissue perfusion
related to reduced coronary blood flow from
coronary thrombus and atherosclerotic plaque
• Acute pain related to myocardial ischemia as
evidenced by severe chest pain and tightness,
radiation of pain to the neck and arms
• Anxiety related to perceived threat of death,
possible lifestyle changes as evidenced by
fearful attitudes, frequent questioning

43. • Cardiac rehabilitation
phase 1- hospital
pahse 11- early recovery- 2-12 wk
phase 111- late recovery- long term
maintanece programme