Myocardial infraction or Heart attack are terms used anonymously, but the preferred term is MI. In an MI an area of the myocardium is permanently destroyed. MI is usually caused by reduced or decreased blood flow in a coronary artery due to rupture of an atherosclerotic plaque and subsequent occlusion of the artery by a thrombus. Myocardial infarction (MI) death of the cells of an area of the heart muscle (myocardium) as a result of oxygen deprivation, which in turn is caused by obstruction of the blood supply; commonly referred to as a “heart attack.” MI refers to the processes by which myocardial tissue is destroyed in regions of the heart that are deprived of an adequate blood supply because of reduced coronary artery blood flow. Eighty percent to 90% of all acute MI are secondary to thrombus formation. When thrombus develops , perfusion to the myocardium distal to the occlusion is halted, resulting in necrosis.The myocardium receives its blood supply from the two large coronary arteries and their branches.  Occlusion of one or more of these blood vessels (coronary occlusion) is one of the major causes of myocardial infarction.  The occlusion may result from the formation of a clot that develops suddenly when an athermanous plaque ruptures through the sub layers of a blood vessel, or when the narrow, roughened inner lining of a scleroses artery leads to complete thrombosis.  The acute MI process takes time. Cardiac cells can withstand in ischemic conditions for approximately 20 minutes before cellular death begins. The earliest tissue to become ischemic is the sub endocardium (the innermost layer of tissue in the cardiac muscle) If ischemia persists, it takes approximately 4 to 6 hours for the entire thickness if the heart muscle to become necrosis.

1. MYOCARDIAL INFRACTION ( MI)
OR HEART ATTACK

2. INTRODUCTION
• Myocardial infraction or Heart attack are terms used
anonymously, but the preferred term is MI.
• In an MI an area of the myocardium is permanently
destroyed.
• MI is usually caused by reduced or decreased blood
flow in a coronary artery due to rupture of an
atherosclerotic plaque and subsequent occlusion of
the artery by a thrombus.

4. •Myocardial infarction (MI) death of the cells of a
n area of the heart muscle (MYOCARDIUM) as a re
sult of oxygen
deprivation, which in turn is caused by obstruct
ion of the blood supply; commonly referred to a
s a “heart attack.”

6. NON MODIFIABLE RISK FACTORS

7. MODIFIABLE RISK FACTORS

8. ETIOPATHOPHYSILOGY
• MI refers to the processes by which myocardial tissue
is destroyed in regions of the heart that are deprived
of an adequate blood supply because of reduced
coronary artery blood flow.
• Eighty percent to 90% of all acute MI are secondary
to thrombus formation. When thrombus develops ,
perfusion to the myocardium distal to the occlusion is
halted, resulting in necrosis.

9. ETIOPATHOPHYSILOGY
• The myocardium receives its
blood supply from the two large coronary arteries and their bran
ches.
• Occlusion of one or more of these blood vessels (CORONARY
OCCLUSION) is one of the major causes of myocardial infarction.
• The occlusion
may result from the formation of a clot that develops suddenly w
hen an athermanous plaque ruptures through the sub
layers of a blood vessel, or when the narrow, roughened inner lin
ing of a scleroses artery leads to complete thrombosis.

11. ETIOPATHOPHYSILOGY
• The acute MI process takes time. Cardiac cells can
withstand in ischemic conditions for approximately
20 minutes before cellular death begins.
• The earliest tissue to become ischemic is the sub
endocardium (the innermost layer of tissue in the
cardiac muscle)
• If ischemia persists, it takes approximately 4 to 6
hours for the entire thickness if the heart muscle to
become necrosis.

12. AREAS OF THE NECROSIS ( WHITE ARROW)

13. CLINICAL FEATURES OF MYOCARDIAL
INFRACTION
1. Cardiovascular clinical features:
A) Chest pain : chest pain occurs suddenly, severe immobilizing
chest pain that not relieved by rest ,position change, and
medications.
B) Increased jugular venous distention
C) BP may be elevated because of sympathetic stimulation or
decreased BP because of decreased contractility, development if
cariogenic shock
D) Decrease pulse rate
E) ST- segment and T-wave changes, ECG may show tachycardia,
bradycardia, or dysrhythmias.

14. Increased jugular venous distention and ST- segment
and t-wave changes in ECG

15. PULMONARY CLINICAL FEATURES
•Shortness of breath (SOB)
•Dyspnea, tachypnea, and crackles if MI has
caused pulmonary congestion.
•Pulmonary edema

16. GASTRO- INTESTINAL CLINICAL FEATURES
• Nausea and vomiting

17. •Genitourinary : Decreased urinary output may
indicate cariogenic Shock
• Skin : Cool ,clammy, diaphoretic, and pale
appearance on skin.
•Neurologic symptoms : Anxiety, restlessness,
and light headiness
•Psychological : Fear with feeling of impending
doom or patient may deny that anything is
wrong.

18. COMPLICATIONS
1. Dysrhythmias ( the most common
complications after an MI in 80% of MI cases.
2. Acute pulmonary edema
3. Heart failure
4. Cariogenic shock
5. Papillary muscle dysfunction
6. Pericarditis and cardiac tamponed

19. Assessment and diagnostic findings
• The diagnosis of an acute myocardial infarction
(MI) is typically based upon the history,
electrocardiogram, and cardiac enzymes,
particularly serum troponins and creatine
kinase MB fraction (CK-MB).

20. Assessment and diagnostic findings
• The diagnosis of MI is generally based on the
presenting symptoms, the ECG, and laboratory test
results (e.g. serial cardiac biomarker valve)
• Patient history

21. ELECTROCARDIOGRAM OR ECG
The ECG provides information that assists in diagnosing
acute MI and It should be obtained within 10 minutes from the
patient a reports chest pain.

22. Echocardiogram
• The echocardiogram is a standard tool in the management of
patients with acute myocardial infarction (MI). The role of
echocardiography in establishing the diagnosis, location,
and extent of MI.

23. LABORATORY TESTS
• Laboratory tests called “CARDIAC
BIOMARKERS” are used to diagnose AMI.
• Creatine kinase –MB or CK-MB, myoglobin
and Troponin T or I

24. MEDICAL MANAGEMENT CLIENT WITH MI
The goal of medical management is to
1. Minimize myocardial damage
2. Preserve myocardial function and prevent
complications
3. Minimizing myocardial damage is also reducing
myocardial oxygen demand and increasing oxygen
supply.

27. PHARMACOLOGIC THERAPY
• The patient with suspected MI given Aspirin , Morphine
sulphate •and Beta blockers.
• Thrombolytic thearpy : Thrombolytic are usually
administered IV, although some may also be given directly
into the coronary artery in cardiac catheterization.
• The purpose of thrombolytic therapy is to dissolve and lyse
thrombus in a coronary artery allowing blood to flow through
the coronary artery again (reperfusion), minimizing the size
of the infraction and preserving ventricular function.

28. • Thrombolytic therapy should not be used if the patient is
bleeding or has a bleeding disorders.
• To be effective, thrombolytic must be administered as early as
possible after the onset of symptoms that indicate an acute MI,
generally within 3 to 6 hours.
Contraindications of thrombolytic therapy such as:
1. Previous hemorrhagic stroke
2. Known intracranial tumor
3. Active internal bleeding
4. Severe uncontrolled hypertension
5. Recent head injury
6. current use of anticoagulants

29. • Analgesics : Morphine sulfate administered in IV
boules to reduce pain and anxiety.
• The cardiovascular response to morphine is
monitored carefully particularly BP and respiratory
rate.
• Angiotensin-converting enzyme inhibitors (ACE
inhibitors)

30. EMERGENT PERCUTANEOUS CORONARY
INTERVENTION
1. Coronary artery bypass graft ( CABG)
2. Percutaneous transluminal coronary
angiography ( PTCA)

31. CORONARY ARTERY BYPASS GRAFT ( CABG)

32. PERCUTANEOUS TRANSLUMINAL CORONARY
ANGIOGRAPHY ( PTCA)

33. CARDIAC REHABILITATION

34. AREAS OF CARDIAC REHABILITATION

35. AREAS OF CARDIAC REHABILITATION
•Smoking cessation
• Lipid management
•Weight control
•Blood Pressure control
• Improve exercise tolerance
• Symptoms control Psychological well-being
/stress management

37. NURSING MANAGEMENT FOR A PATIENT WITH
ACUTE MI

38. NURSING MANAGEMENT FOR A PATIENT WITH
ACUTE MI
• Achieving a balance between myocardial oxygen
supply and demand
• This are achieved via oxygen administration and
medication (Nitroglycerin)
• Prevention of complications
• Continuous monitoring of cardiac functions
• Continuous ECG monitoring
• Hemodynamic monitoring

39. NURSING MANAGEMENT FOR A PATIENT WITH
ACUTE MI
• Monitor and record intake and urine output
• Closely monitor and prevent complications associated with
MI particularly dysrhythmia and cardiogenic shock
• Provide emotional and psychological support
• Explain and provide adequate information and knowledge
about disease condition and treatment process
• Motivate regarding active involvement in cardiac
rehabilitation.

40. RISK FACTORS MODIFICATION
•Daily fat intake less than 309 % of total calories
•Maintenance of serum cholesterol level
•Maintain LDL levels less than 70 mg/dl
• Stop smoking and reduce daily salt intake
• Control Hypertension and diabetes
• Increase physical activity and reduce weight

41. NURSING DIAGNOSIS
1. Ineffective cardiac tissue perfusion related to
reduced coronary blood flow from coronary
thrombus and atherosclerotic plaque
2. Risk for imbalanced fluid
3. Death of anxiety
4. Deficient knowledge about post-MI and self
care