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HELLO EVERYONE

DR AKHILESH SHRIVASTAVA
MYOCARDIAL INFARCTION
MYOCARDIAL INFARCTION

MI is defined as a diseased condition which is caused by reduced blood flow in


a coronary artery due to atherosclerosis & occlusion of an artery by an
embolus or thrombus.

MI or heart attack is the irreversible damage of myocardial tissue caused by


prolonged ischaemia & hypoxia.
LOCATION / TYPES OF MYPCARDIAL INFARCTION
1According to anatomic region of left ventricle invoved
Obstruction of the left anterior descending artery (LAD) results in anterior or septal wall MI.
Obstruction of the circumflex artery results in posterior wall MI or lateral wall MI.
Obstruction of the right coronary artery results in inferior wall MI.
2According to degree of thickness of ventricular wall involved:
Transmural (full thickness)
Laminar (subendocardial)
3. According to age of infarcts:
Newly formed (acute, recent, fresh)
Advanced infarcts (old, healed, organised)
ETIOLOGY
 NON-MODIFIABLE RISK FACTORS
AGE: More than 40 years.
FAMILY HISTORY: Myocardial infarction can be inherited from parents to children.
GENDER: Myocardial infarction is 3 times more in men than women.
MODIFIABLE RISK FACTORS
PATHOPHYSIOLOGY
Causative factor: Obesity ,DM,SMOKING ,HT etc..
Atherosclerosis of coronary artery Narrowing of lumen ed heart insufficient blood flow to
myocardium Contractility ed O2 demand of myocardial cells Inadequate creates an O2 deficit
Blood supply myocardial cell death inflammation
Oliguria CK-MB & Troponine released Fever
Anaerobic glycolysis Accumulation of lactic acid Irritation of myocardial nerve fibers
Transmission of pain to myocardium Chest pain & radiation towards shoulder & arm
Stimulation of vomiting SNS Stimulation center increased Nausea & Vomiting catecholamine
Diaphoresis Increased (perfuse sweating) Heart Rate Cold & Clammy skin “Cold Sweat”
PAIN Characteristics: Severe, immobilizing chest pain. Usually described as heaviness,
pressure, tightness, burning. Location: Substernal, Retrosternal or Epigestric.
Radiation: It may radiate to neck, jaw, arm or back. Duration: Lasts for 20 minutes or more.
NAUSEA & VOMITING Stimulation of vomiting center by severe pain causes nausea &
vomiting.
FEVER 100.4 to 102.2°F It is due to inflammatory process caused by Myocardial cell death.
CARDIOVASCULAR MANIFESTATIONS-
Hypotension Decrease cardiac output Shock Urine output (Oliguria): <30ml/day.
Dyspnoea
DIAGNOSTIC TESTS
Electrocardiogram- ECG provides information that assists in diagnosing acute MI.

The classic ECG changes are- T wave inversion /ST segment elevation /Abnormal Q wave

ANGIOGRAPHY To detect percentage of blockage & type of MI.

CHEST X-RAY To detect cardiomegaly.


Positron emission tomography- (PET scan) -It is used to evaluate cardiac metabolism & to
assess tissue perfusion.
DRUG THERAPY IN MYOCARDIAL INFRACTION
Pharmacological therapy in MI has following objectives.
1.To reduce pain, anxiety and apprehension .
2.Oxygenation .
3.Maintenance of blood volume, tissue perfusion, and microcirculation .
4.correction of acidosis. 5.Prevention and treatment of arrhythmias.
6.To manage cardiac output .
7.Prevention of thrombus extension, embolism, venous thrombosis
8.Thrombolysis and reperfusion.
9.Prevention of remodeling and subsequent CHF
10.Prevention of future attacks a. platelet inhibitors. b. beta blockers c. control of
hyperlipidemia .
 1.To reduce pain anxiety and apprehension 1. After pain is not relieved by 3 doses of GTN given 5 min. apart ,
an opioid analgesic [morphine /pethidine] or diazepam is administered parentally.
 Prevention and treatment of arrhythmias. Prophylactic i.v. infusion of beta blockers as soon as the MI patient
is seen ,reduces the incidence of arrhythmia and mortality . Beta blockers used early in evolving MI can
reduce the infract size and complications. Tachyarrhythmias may be treated with i.v lidocaine, procainamide,
or amiodarone.

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