This document discusses myocardial infarction (MI), also known as a heart attack. It defines MI as being categorized based on anatomy and diagnosis as either transmural or subendocardial, and presenting with ST elevations (STEMI) or not (NSTEMI). It lists modifiable and non-modifiable risk factors for MI and describes the signs, symptoms, causes, diagnostic methods, pathophysiology, complications, management, treatment, and prevention of heart attacks.

3. Classification of MI
Can be subcategorized by anatomy and clinical diagnosis
information:
1-Anatomic:
Transmural and subendocardial
2-Diagnostic:
ST elevations (STEMI) and non (NSTEMI).

5. Risk factors for AMI:
(modifiable)
o High Blood Pressure
o High Triglyceride and cholesterol
o Obesity and physical in activity
o Diabetes or High Blood Sugar
o Excessive intake and saturated fats, carbohydrates and salt.
o Stress
o Drugs
o smoking

6. (Non modifiable)
• Age> 45 y
• Gender: men are more susceptible than
predominant women
• Family history.

7. Causes of AMI:
 Bad Cholesterol, also called low density lipoprotein
(LDL)
 Saturated Fats
 Trans Fat

8. Signs of AMI:
 anxiety
 cough
 dizziness
 fast heart rate
 heaviness in or across the chest
 pain in the chest, back, jaw, and other areas of the upper
body
 shortness of breath
 sweating
 Nausea and vomiting

9. Symptoms in some women may
differ from those usually in men
e.g many women have
predominant symptoms of
heartburn , malaise, heart beat
abnormalities
Cough, loss appetite, ignoring
such symptoms may cause
treatment delays more damage
heart tissue.

10. MI are the leading cause of death in the US ,
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.

11. The survival rate for those hospitalized due to MI has
reached approximately 95% .
This is the result of advancements made in model
medical technology.

13. pathophysiology
• Ischemic develops when there is an increased oxygen
demand or decreased supply of oxygen .
• Ischemic can develop within 10 sec and if it lasts longer
than 20 min , irreversible cell and death occur.
• Myocardial cell death begins at the endocardium. The
area must distal to the arterial blood supply.

14. As vessel occlusion continous cell death spreads to the
myocardium and evantually to the epicardium
Severity of MI depends on three factors:
 level of occlusion
 length of time of occlusion
 presence or absence of collateral circulation

16. Complications:
Depends on the size, location, duration of lesions.
Within minutes to 3 days:
• Arrhythmia
• Cardiac shock
• Thrombotic complication
• Rupture of the heart

17. Complications
3 to 14 days:
• Acute fibrinous or hemorrhage precarditis over infarct
area .
After weeks or months:
• Chronic heart failure
• Cardiac aneurysm, which may rupture producing
hemopericardium and death

19. diagnostic methods include:
 troponin test – to check for heart damage
 electrocardiogram – to measure the heart’s electrical
activity
 stress test – to check how your heart reacts to certain
situations, such as exercise.

20.  Blood test
 X- ray
 Ejection fraction
 Creatine phosphatase elevated for
first hours

21. MANAGEMENT
Analgesics
Thrombolytic therapy
Anticoagulant and antiplatelet medications
Other medications such as ( beta adrenergic
blocking agent) and Diazepam.

22. Treatment
• The immediate goal for any AMI is to restore normal
coronary blood flow to vessels and salvage myocardium
• There are a variety of myocardial and medical therapies
to treat a MI.

23. General treatment for the MI patient
• Morphine
• Oxygen
• Nitroglycerin
• Aspirin

24. 
Get regular medical checkup
Control your blood pressure
Check your cholesterol
Do not smoke
Excercise regularly
Maintain in healthy weight
Manage stress
Prevention

25. THANK YOU