Acute myocardial-infraction

1. This presentation on
Acute Myocardial Infraction
Presented By
Dr. Swarna Lata Das
Department of Medicine
Gazi Medical College & Hospital
Khulna,Bangladesh

2. Objectives
Define and Understand the epidemiology of MI and
how they are classified.
Will be able to identify the risk factors associated with
MI’s.
Will be able to recognize sign and symptoms of acute
MI and what the appropriate investigation are.
Understand the treatment options available to treat MI.

3. Definition
Acute Myocardial Infraction may be defined as necrosis of
myocardium due to impaired blood supply according to the need
of tissue.
MI is also known as heart attack.
Contractive function stops in the necrotic areas of the heart.
Ischemia usually occurs due to blockage of the coronary
vessels.
This blockage is often result of thrombus that is superimposed
on an ulcerated or unstable atherosclerotic plaque for motion in
the coronary artery.

4. Area affected in MI
MI’s are described by the area of occurrence.
-Anterior wall of LV.
-Inferior wall of LV.
-Lateral wall of LV.
-Posterior wall of LV.
-Rt Ventricle.

5. Events occurs in MI
Ischemia
-Occurs in outer most areas. Myocardial tissue is
viable if no further infarction.
Injury
-Viable tissue found between ischemia and infracted
areas.
Infraction
-Occurs in centre area. Dead tissue that turn into scar.

6. Events occurs in MI contd’
A. Ischemia
B. Injury
C. Dead

7. MI Classifications
MI can be subcategorized by anatomy and
clinical diagnostic information.
Anatomic
- Transmural.
-Sub endocardial.
Diagonostic
-ST elavations (STEMI)
-Non ST elavations (NSTEMI)

8. Risk Factors
The present of any risk factor is associated with
doubling the risk of an MI.
Non Modifiable
1.Age
2.Gender
3.Family History

9. Risk Factors contd’
Modifiable
Smoking
- Tobacco use increases the risk of coronary artery
disease and that is two to six times more than non
smokers.
- Nicotine increases platelet thrombus adhesion and
vessel inflammation.

10. Diabetes and 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.

11. Hyperlipidemia
Elevated levels of
cholesterol, LDL’s or
triglycerides are
associated with the
increased risk of coronary
plaque formation and MI.
Almost 50% of the
population has some form
of dyslipidemia.

12. Obesity and Physical
inactivity
 Mortality rate is high form
coronary artery disease in
those who are obese.
 Some evidence shows that
those who carry their
weight in their abdomen have
a higher incidence of
coronary artery disease.
 Physically inactive people
have lower HDL levels
with higher LDL levels and
increase in clot formation.
formation.

13. Dietary Habit
Lack of-
Fresh food
Vegetables
Poly saturated fatty
acids.

14. Alcohol

15. Pathophysiology

16. Signs and Symptoms
Symptoms
Prolonged cardiac pain-chest ,
thoracic, arms,
epigastrium,neck region or
back.
Anxiety and fear of impending
death.
Nausea and Vomiting.
Breathlessness.
Collapse.

17. Signs
Sings of Sympathetic activation
-Pallor
-Sweating
-Tachycardia
Sings of vagal activation
-Vomiting
-Bradycardia
Sings of tissue damage
-Fever

18. Signs contd’
Sings of impaired myocardial
function
-Hypotension ,Oliguria ,cold
peripheries
-Narrow pulse pressure
-Raised JVP
-Third heart sound
-Quite first heat sound
-Diffuse apical impulse
-Lung crepitations.
Sings of complications
-Mitral regurgitation
-Pericardities

19. Investigations
Electrocardiography
Plasma cardiac markers
Blood tests
Chest x-ray
Echocardiography

20. ECG changes in MI
ST elevation followed by T wave inversion
Pathological Q wave development
If abnormality occurs in v1 to v4-anteroseptal MI.
If abnormality shows in v4 to v6 and aVL and lead I
– anterolateral MI.
If abnormalities occur in leads II,III and aVF- Inferior
MI.

21. Serum Cardiac Markers
Myocardial cells produce
certain portions and
enzymes associated with
cellular functions.
When cell death occurs
these cellular enzymes are
released into the blood
stream.
Mostly done Cardiac
Markers are
1) Troponin
2) CK-MB

22. Cardiac Markers

23. Cardiovascular Changes in MI
Initially the BP and pulse may be elevated.
Later BP will drop due to decreased cardiac
output.
Urine output will decrease.
Lung sound will change to crackles.
Jugular veins may become distended and
have obvious pulsations.

24. Treatment Option
Immediate hospitalization where
defibrillation facility is available.
High flow oxygen
Intravenous access
ECG monitoring
Aspirin 300mg chewed and
clopidogrel 600mg oral.
Sublingual glyceryl trinitrate
Intra-venous analgesic
Beta blokers
ACE inhibitor
Thrombolytic or Anticoagulant

25. Treatment Option contd’
If ST elevated MI- Thrombolysis with streptokinase
1.5 million U in 100ml of saline given as an
intravenous infusion over 1 hour. Alteplase and
retiplase are the other option.
If non ST elevated MI- low molecular weight heparin.

26. Others Options
Percutaneous intervention

27. Others options contd’
Cardiac Catheterization

28. Others options contd’
Coronary artery bypass graft.

29. Long Term Care
Smoking Cessation and life style modification.

30. Long Term Care contd’
Aspirine, Beta blockers and clopidogrel are taken for indefinite period.

31. Long Term Care contd’
Lipid lowering medication along with diet modification.

32. Thank you all for patience
hearing.