This document provides an overview of myocardial infarction (MI), also known as a heart attack. It defines MI as diminished blood supply and cell damage in the heart muscle. Risk factors include age, gender, family history, smoking, diabetes, hypertension, hyperlipidemia, obesity, and physical inactivity. Symptoms range from chest pain to breathlessness. Diagnosis involves ECGs, cardiac enzyme levels, and cardiac imaging. Treatment depends on whether the MI is STEMI or NSTEMI and may include medications, fibrinolytic therapy, angioplasty, and lifestyle changes to modify risk factors.

1. Myocardial Infarction
Dr. Abdur Rehan
Dr. Muhammad Aamir Iqbal
West Medical Ward

2. Definition
• 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.

7. 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).

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

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

10. 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.

11. 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.

12. Hyperlipidemia
• Elevated levels of cholesterol, LDL’s or
triglycerides are associated with the
increased risk of coronary plaque
formation and MI.

13. 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.

14. 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.

15. 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

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

17. Clinical Presentation
• Retrosternal pain, more severe and lasts
longer i.e. > 30 min, present at rest,
heavy, squeezing & crushing, stabbing or
burning radiating to arms, back, lower jaw,
neck & epigastrium.
• Associated with nausea, vomiting, anxiety
& palpitation.
• Painless STEMIs in diabetics in older age
group

18. • Sudden onset of breathlessness
• Sudden loss of consciousness &
confusion state

19. Diagnostics
• Typical chest pain
• ECG
• Serum cardiac enzymes
• Cardiac imaging

20. Normal Sinus Rhythm

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. Localization of MI
• ST elevation only
• Inferior wall- II, III, aVF
• Lateral wall- I, aVL, V4-V6
• Anteroseptal- V1-V3
• Anterolateral- V1-V6
• Right ventricular- RV4, RV5
• Posterior- R/S ratio >1 in V1 and T wave
inversion

29. 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

30. CPK
• Creatine Phosphokinase
• CPK-MB more specific for STEMI
• Begin to rise 3 to 12 hours after acute MI.
• Peak in 24 hours
• Return to normal in 2 to 3 days

31. Troponin
• Troponin-T & Troponin-I
• 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.

32. Serum Cardiac Markers

33. 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

34. Pre Hospital Management
• Aspirin 300 mg stat
• S/L nitrates 0.4 mg up to 3 doses
• Analgesia morphine 5-10 mg IV +
metaclopramide 10 mg IV

35. In Hospital
• High flow O2 .
• Analgesia morphine 5-10 mg IV +
metaclopramide 10 mg IV.
• S/L GTN
• IV β-blockers metoprolol 5 mg every 5 min
for 3 doses, 15 min after the last IV dose
oral regimen is started 50 mg/6h for 48 hrs
followed by 100 mg/12h.

36. Fibrinolytic Therapy
• Indicated for patients with STEMIs.
• Should be given within 12 hours of
symptom onset.
• Fibrinolytics will break down clots found
within the vessles

37. Types of fibrinolysis
• Fibrin specific agents
tPA, tenecteplase, reteplase. rtPA indicated if
patients received previously SK > 4 days or
reacted to SK, 15 mg loading followed by 50
mg IV over 30 min followed by 35 mg over
60 min. rPA double bolus regimen 10 MU
bolus over 2 min followed by 2nd 10 MU over
30 min. TNK single IV bolus of 0.53 mg/kg
over 30 min. UFH is usually indicated after
thrombolysis.

38. • Non-fibrin specific agent
1.5 MU SK over 1h in 100 ml N/S. S/E
nausea, vomiting, hemorrhage, stroke,
disarrythmias & allergic reactions. No
indication of UFH after SK

39. Contraindications
Absolute
•H/O CVA hemorrhage , Non-hemorrhagic
stroke
•Marked hypertension systolic > 180 &
diastolic > 110 at presentation
•Suspicion of aortic dissection , Active
internal bleeding

40. Contraindications
Relative
•Current use of anticoagulant , Recent
surgical procedure
•Prolonged or traumatic CPR
•Bleeding diathesis, pregnancy, diabetic
retinopathy, peptic ulcer disease

41. Hospital phase management
Activity:
•First 12 hrs. Complete bed rest
•12-24 hrs. Resume upright posture by
hanging their feet over the side of the bed &
sitting in the chair
•By the 2nd & 3rd day patients are walking in
the room with increasing duration &
frequency and may take shower or bath.
•By 3rd day after infarction patient should
increase their walk progressively to 600 ft 3
times a day.

42. Diet:
•Either nothing or only clear fluids by mouth
for the 1st 4-12h to prevent emesis or
aspiration.
•Food enriched with K, Mg and fibers but
low in Na.
Bowels:
•Diet rich in bulk and the routine use of stool
softner to prevent constipation
Sedation:
•Benzodiazepines

43. Subsequent Management
• Daily exam for complication
• Daily 12 lead ECG, cardiac enzymes for 2-
3 days
• Prophylaxis against thrombolysis, UFH
until fully mobilized. If large anterior MI
consider warfarin for 3 months against
systemic embolism from mural thrombus.
Daily low dose Aspirin 75-150 mg
indefinitely
• Start oral β-blocker, Metoprolol 50 mg/6h
if contraindicated Verapamil Continuous
ACE inhibitor

44. • Modify risk factors, discourage smoking,
encourage exercise, treat DM, HTN,
hyperlipidemia
• Discharge after 5-7 days
• May return to work after 2 months
• Few occupations should not be restarted
after MI like pilots, drivers, divers, air
traffic controllers
• Avoid air travel for 2 months
• Start Statin

45. 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.

46. Complications
• Recurrent ischemia or failure to reperfuse
• Cardiac arrest ,cardiogenic shock
• Arrythmias
• LVF,RVF
• Pericarditis
• DVT,PE,systemic embolism

47. • Cardiac tamponad
• MR,VSD
• Dressler's syndrome
• LV aneurysm