This document provides an overview of acute myocardial infarction (AMI or heart attack). It defines AMI as necrosis of heart muscle due to inadequate blood supply following coronary occlusion. The causes include lifestyle factors, physiological characteristics, disease conditions, and personal characteristics. The pathophysiology involves prolonged ischemia leading to cellular damage and dysfunction. Symptoms include chest pain and other signs of inadequate circulation. Diagnostic evaluation involves cardiac enzymes, electrocardiogram, imaging, and angiography. Management consists of oxygen, thrombolysis, analgesics, vasodilators, medications, and sometimes surgery. Nursing care addresses pain, perfusion, breathing, mobility, and activity tolerance. Complications can include heart failure and abnormal heart rhythms.

1. MR.GOPAL ,..MSC (N),
MEDICAL SURGICAL NURSING
ASSISTANT PROFESSOR
GANGA COLLEGE OF NURSING
COIMBATORE

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3. CONTENT OVERVIEW
• ANATOMY & PHYSIOLOGY OF THE HEART
• INTRODUCTION
• DEFINITION
• CAUSES
• PATHOPHYSIOLOGY
• SYMPTOMS
• DIAGNOSTIC EVALUATION
• MANAGEMENT
• COMPLICATIONS

4. •

5. INTRODUCTION
Acute myocardial infarction (AMI) is
necrosis of heart muscle due to inadequate
blood supply following an acute coronary
occlusion. This occlusion is usually due to
plaque rupture or fissuring with
superimposed thrombosis. Rarely, this may
result from coronary spasm, coronary
embolism or vasculitis.

6. DEFINITION
A Myocardial infarction occurs as a
result of sustained ischemia, causing
irreversible myocardial cell death (necrosis).
A heart attack is when blood vessels
that supply blood to the heart are blocked,
preventing enough oxygen from getting to
the heart. This causes the muscles to die.

7. CAUSES
LIFE STYLE
• Tobacco smoking
• Excessive alcohol
• Physical Inactivity
• High saturated diet and cholesterol

8. CAUSES
PHYSIOLOGICAL CHARACTERISICS
(MODIFIABLE)
• Elevated LDL cholestrol
• Low plasma HDL cholestrol
• Elevated plasma triglyceride
• Hyperglycemia
• Obesity
• Thrombogenic factors

9. CAUSES
DISEASE CONDITION
• Atherosclerosis
• Coronary thrombosis/ embolism
• Platelet aggregation
• Coronary artery stenosis/ spasm
• Shock /haemorrhage
• CKD
• Complication from heart surgery

10. CAUSES
PERSONAL CHARACTERISTICS
(NON MODIFIABLE)
• FAMILY HISTORY OF CHD
• MALE GENDER
• OLDER AGE

11. PATHOPHYSIOLOGY
OCCLUSION OF CORONARY ARTERY
PROLONGED ISCHEMIA
DECREASED OXYGEN, GLYCOGEN
AND ATP STORES

12. SHIFTING OF CELLULAR
METABOLISM FROM AEROBIC
PROCESS TO ANEROBIC PROCESS
PRODUCTION OF HYDROGEN ION
AND LACTIC ACID
CELLULAR ACIDOSIS
INCREASED CELL VULNERABILITY
TO FURTHER DAMAGE

13. RELEASE OF INTRACELLULAR
ENZYME THROUGH DAMAGED CELL
MEMBRANE INTO INTERTITIAL
SPACE
DECREASED IMPULSE CONDUCTION
AND MYOCARDIAL CONTRACTILITY
DECREASED CARDIAC OUTPUT,
STROKE VOLUME, BLOOD
PRESSURE AND TISSUE PERFUSION

14. SYMPTOMS
Chest pain (central chest pain may not be the
main symptom):
• Three quarters of patients present with
characteristic central or epigastric chest pain
radiating to the arms, shoulders, neck, or jaw.
• The pain is described as substernal pressure,
squeezing, aching, burning, or even sharp pain.
• Radiation to the left arm or neck is common.
• Chest pain may be associated with sweating,
nausea, vomiting, dyspnoea, fatigue and/or
palpitations.

15. • Anxiety & Fainting
• Cough
• Light-headedness, dizziness
• Nausea and vomiting
• Palpitations (feeling like your heart is
beating too fast or irregularly)
• Shortness of breath
• Sweating, which may be extreme.
• Pale skin

16. • Diaphoresis (an excessive form of
sweating),
• Light-headedness, and
• Palpitations
• Loss of consciousness
• inadequate blood flow to the brain
• and cardiogenic shock.
• Sudden death
• due to the development of ventricular
fibrillation.

17. DIAGNOSTIC EVALUATION
• Patient history
• ECG- ST elevation signifying ischemia.
• Cardiac enzymes and isoenzymes. CPK
MB (isoenzyme in cardiac muscle): Elevates
within 4–8 hrs, peaks in 12–20 hrs, returns to
normal in 48–72 hrs.
• LDH. Elevates within 8–24 hrs, peaks within 72–
144 hrs and may take as long as 14 days to
return to normal. An LDH1 greater than
LDH2 (flipped ratio) helps confirm/diagnose MI
if not detected in acute phase.

18. • Troponins. Troponin I (cTnI) and troponin T
(cTnT): Levels are elevated at 4–6 hr, peak at
14–18 hr, and return to baseline over 6–7
days. These enzymes have increased
specificity for necrosis and are therefore
useful in diagnosing postoperative MI when
MB-CPK may be elevated related to skeletal
trauma.
• Electrolytes. Imbalances
of sodium and potassium can alter
conduction and compromise contractility.
• WBC. Leukocytosis (10,000–20,000) usually
appears on the second day after MI because
of the inflammatory process.

19. • ESR : Rises on second or third day after MI,
indicating inflammatory response.
• ABGs/pulse oximetry: May indicate hypoxia or
acute/chronic lung disease processes.
• Lipids (total lipids, HDL, LDL, VLDL, total
cholesterol, triglycerides,
phospholipids): Elevations may reflect
arteriosclerosis as a cause for coronary narrowing
or spasm.
• Chest x-ray: May be normal or show an enlarged
cardiac shadow suggestive of HF or
ventricular aneurysm.
• Two-dimensional echocardiogram: May be done to
determine dimensions of chambers,
septal/ventricular wall motion, ejection fraction
(blood flow), and valve configuration/function.

20. • Nuclear imaging studies: Persantine or
Thallium: Evaluates myocardial blood flow
and status of myocardial cells, e.g.,
location/extent of acute/previous MI.
• Coronary angiography: Visualizes
narrowing/occlusion of coronary arteries and
is usually done in conjunction with
measurements of chamber pressures and
assessment of left ventricular function
(ejection fraction). Procedure is not usually
done in acute phase of MI unless angioplasty
or emergency heart surgery is imminent.

21. • Digital subtraction angiography
(DSA). Technique used to visualize status of
arterial bypass grafts and to detect peripheral
artery disease.
• Magnetic resonance imaging (MRI). Allows
visualization of blood flow, cardiac chambers
or intraventricular septum, valves, vascular
lesions, plaque formations, areas of
necrosis/infarction, and blood clots.
• Exercise stress test. Determines cardiovascular
response to activity (often done in conjunction
with thallium imaging in the recovery phase).

22. • Myoglobin: The myoglobin level can
elevate within 1 to 2 hours of acute MI
and peaks within 3 to 15 hours.
• Troponin: (troponin T and troponin I):
• Troponin I levels rise in about 3 hours,
peak at 14 to 18 hours, and remain
elevated for 5 to 7 days.
• Troponin T levels rise in 3 to 5 hours and
remain elevated for 10 to 14 days

24. MEDICAL MANAGEMENT
• OXYGEN THERAPY
• THROMBOLYTIC THERAPY
– Urokinase
– Streptokinase
• ANALGESICS THERAPY
– Morphine
• VASODILATOR THERAPY
– Nitroglycerin

25. • ACE INHIBITORS
– Captopril
– Enalapril
• BETA-ADRENERGIC BLOCKING AGENT
– Propenolol
• CALCIUM CHANNEL BLOCKERS
– Nifedipine
• ANTOCOAGULANT THERAPY
– Heparin

26. SURGICAL MANAGEMENT
• CABG (CORONARY ARTERY BYPASS GRAFT)
• PTCA (PERCUTANEOUS TRANSLUMINAL
CORONARY ANGIOPLASTY)
• ATHERECTOMY
• TRANSMYOCARDIAL LASER
REVASCULARIZATION

27. NURSING DIAGNOSIS
• Acute pain on chest related to myocardial
ischemia
• Ineffective peripheral tissue perfusion related
to decreased oxygenation
• Decreased cardiac output related to decreased
cardiac contractility
• Ineffective breathing pattern related to
increased effort of breath
• Impaired physical mobility related to chest pain
• Activity intolerance related to chest pain

28. COMPLICATION
• Heart failure. If a large area of the heart
muscle is damaged then the pumping ability
of the heart may be reduced.
• Abnormal heart rhythms may occur if the
electrical activity of the heart is affected.
• Renal / Respiratory failure