Myocardial infarction, or heart attack, occurs when blood flow to the heart is blocked, damaging heart muscle. It is usually caused by a blood clot forming in one of the coronary arteries. A heart attack can lead to damage or death of heart muscle depending on how much of the heart is affected and for how long. Diagnosis involves assessing symptoms, electrocardiogram changes, and cardiac enzyme levels. Treatment focuses on restoring blood flow through clot-busting drugs or angioplasty, along with medications, monitoring, and lifestyle changes to prevent future heart attacks.

1. Myocardial Infarction
ASIS KUMAR SAMAL
Msc Nursing 1st
year

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 ulcerated or unstable
atherosclerotic plaque formation in the
coronary artery.

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. 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.

10. 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.

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

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

13. 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.

14. Diabetes & Hypertension
• Diabetes not only increases the rate of
atherosclerotic formation in 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.

15. Hyperlipidemia
• Elevated levels of cholesterol 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.

16. 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.

17. 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.
• .

18. Pathophysiology
• Myocardial cell death begins at the
endocardium. The area most distal to the
arterial blood supply
• As vessel occlusion continues cell death
spreads to the myocardium and eventually
to the epicardium.

19. • Severity of the MI depends on three
factors.
– Level of occlusion
– Length of time of occlusion
– Presence or absence of collateral circulation

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

21. 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.

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

23. Nausea and Vomiting
• Not everyone will experience this.
• Vomiting results as a reflex from severe
pain.

24. 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.

25. 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

26. 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

27. Diagnostics
• collecting patient health history,
• 12 lead ECG can help to distinguish
between ST-elevation MI’s and Non-ST-
elevation MI’s.

28. Normal Sinus Rhythm

29. Angina
Stable
• Chest pain caused by the build up of lactic
acid and irritation to the myocardial nerve
fibers.
• Pain is usually relieved with rest and
nitrates.

30. • Pain is caused by vasospasm of the
arteries.
• ST segment elevations will be noted.

31. 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.
• ECG will reveal ST segment depression
and T wave inversion.

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

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

34. STEMI vs. NSTEMI

35. Phases of a STEMI
– 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
– T waves become tall, widened and might be
taller than the R wave.

36. 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.

37. 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

38. 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

39. 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.

40. • Serum electrolyte
• Serum potassium
• Serum sodium
• Serum magnesium
• Cardiac catheterization
•

41. Management
• The ECG is examined for the presence of
ST segment elevations of 1 mV or greater
in contiguous leads.
• 1. Administer aspirin, 160 to 325 mg
chewed.
• 2. After recording the initial 12-lead ECG,
place the patient on a cardiac monitor and
obtain serial ECGs.
• 3. Give oxygen by nasal cannula.

42. • 4. Administer sublingual nitroglycerin
(unless the systolic blood pressure is less
than 90 mm Hg or the heart rate is less
than 50 or greater than 100 beats/minute).
• 5. Provide adequate analgesia with
morphine sulfate. Provide adequate
analgesia with morphine sulfate.

43. Thrombolytic Therapy
• Thrombolytic therapy provides maximal
benefit if given within the first 3 hours after
the onset of symptoms.
• Significant benefit still occurs if therapy is
given up to 12 hours after onset of
symptoms.

44. Primary Percutaneous Transluminal
Coronary Angioplasty (PTCA)
• (PTCA) is an effective alternative to
reestablish blood flow to ischemic
myocardium.
• The nurse must carefully monitor the
patient after a primary PTCA for evidence
of complications

45. INTENSIVE AND INTERMEDIATE
CARE MANAGEMENT
• IV nitroglycerin is continued for 24 to 48 hours.
• Daily aspirin is continued .
• Clopidogrel may be used for patients who are intolerant
of aspirin.
• IV beta blocker therapy should be administered within
the initial hours of the evolving infarction, followed by oral
therapy provided there are no contraindications.
• Beta blockers are one of the few pharmacological agents

46. • Angiotensin converting enzyme inhibitor
• Ca channel blocker
• Cholesterol lowering agent

47. Hemodynamic Monitoring
• Use of a pulmonary artery catheter for
hemodynamic monitoring is indicated in
the patient with MI who has severe or
progressive congestive heart failure or
pulmonary edema, cardiogenic shock,
progressive hypotension, or suspected
mechanical complications.

48. Complications
Vascular Complications
• Recurrent ischemia
• Recurrent infarction
Mechanical Complications
• Left ventricular free wall
rupture
• Ventricular septal rupture
• Papillary muscle rupture
with acute mitral
regurgitation
Myocardial Complications
• Diastolic dysfunction
• Systolic dysfunction
• Congestive heart failure
• Hypotension/cardiogenic
shock
• Right ventricular
infarction
• Ventricular cavity dilation

49. Nursing Diagnoses
• Acute Pain related to oxygen supply and
demand imbalance
• Anxiety related to chest pain, fear of death,
threatening environment
• Decreased Cardiac Output related to impaired
contractility
• Activity Intolerance related to insufficient
oxygenation to perform activities of daily living,
bed rest
• Risk for Injury (bleeding) related to dissolution of
protective clots

50. Nursing Interventions
Reducing Pain
• Handle patient carefully while providing initial care,
starting I.V. infusion, obtaining baseline vital signs, and
attaching electrodes for continuous ECG monitoring.
• Maintain oxygen saturation greater than 92%.
• Administer oxygen by nasal cannula if prescribed
• Encourage patient to take deep breaths may decrease
incidence of dysrhythmias by allowing the heart to be
less ischemic and less irritable; may reduce infarct size,
decrease anxiety, and resolve chest pain.