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Myocardial Infarction- Definition, etiology, pathophysiology, sign and symptoms, diagnosis

MYOCARDIAL INFARCTION

DEFINITION

MI refers to the process by which areas of myocardial cells in the heart are permanently destroyed.

ETIOLOGY

  • Atherosclerosis and occlusion of an artery by an embolus or thrombus.
  • Vasospasm (sudden constriction or narrowing) of a coronary artery
  • Decreased oxygen supply (eg, from acute blood loss, anemia, or low blood pressure);
  • Increased demand for oxygen (eg, from a rapid heart rate, thyrotoxicosis, or ingestion of cocaine)

PATHOPHYSIOLOGY

Risk factors leads to

Atherosclerotic plaque formation in the lumen of coronary arteries that

Stimulate the platelet aggregation and thrombus formation resulting in

Narrowing of lumen of coronary arteries causing

Ischemia to myocardial cells resulting in

Anaerobic metabolism of glycogen causing

Accumulation of hydrogen ions and lactate

Acidosis develops resulting in

Myocardial necrosis

Then Scar tissue replaces healthy tissue resulting in

Impaired myocardial contractility that results in

Decreased cardiac output

It further increases the myocardial demand for oxygen and increase the workload of heart resulting in

Myocardial infarction

 

CLINICAL MANIFESTATIONS

Cardiovascular

  • Chest pain or discomfort
  • Palpitations
  • S3, S4 heart sounds and new onset of murmur
  • Increased jugular venous distention
  • Blood pressure elevated
  • Pulse deficit

Respiratory

  • Shortness of breath
  • Dyspnea
  • Tachypnea

Gastrointestinal

  • Nausea and vomiting

Genitourinary

  • Decreased urinary output

Skin

  • Cool, clammy, diaphoretic and pale appearance
  • Dependent edema

Neurologic

  • Anxiety
  • Restlessness
  • Headache
  • Visual disturbances
  • Altered motor function
  • Changes in level of consciousness

ASSESSMENT AND DIAGNOSTIC FINDINGS

  • PATIENT HISTORY
  • ELECTROCARDIOGRAM – The ECG provides information that assists in diagnosing acute MI. The classic ECG changes are T-wave inversion, ST-segment elevation, and development of an abnormal Q wave.
  • ECHOCARDIOGRAM – The echocardiogram is used to evaluate ventricular function. It can detect hypokinetic and akinetic wall motion and can determine the ejection Fraction.
  • LABORATORY TESTS
  • Creatine Kinase and Its Isoenzymes

°   There are three CK isoenzymes: CK-MM (skeletal muscle), CK-MB (heart muscle), and CK-BB (brain tissue).

°    CK-MB is the cardiac-specific isoenzyme; CK-MB is found mainly in cardiac cells and therefore rises only when there has been damage to these cells.

°    The level starts to increase within a few hours and peaks within 24 hours of an MI.

  • Myoglobin

°   Myoglobin is a heme protein that helps to transport oxygen.

°   The myoglobin level starts to increase within 1 to 3 hours and peaks within 12 hours after the onset of symptoms.

  • Troponin:
    • A protein found in the myocardium, regulates the myocardial contractile process. There are three isomers of troponin (C, I, and T).
    • The increase in the level of troponin in the serum starts and peaks at approximately the same time as CK-MB.
    • However, it remains elevated for a longer period, often up to 3 weeks and it cannot be used to identify subsequent extension or expansion of an MI.

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