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Heart Attack (Myocardial Infarction): Sign, Syptoms, types, Treatment:

February 15, 2020 by dramjad Leave a Comment

Myocardial infarction (Heart Attack):

It refers to localized area of cardiac necrosis due to ischemia. It affects man more than a women. Women are protected against MI during reproductive years, but postmenopausal hormone replacement therapy doesn’t protect women against MI.

  • Myocardial Infarction

Risk factors:

Aging, male gender, hypertension, smoking, DM, Hypercholesrolemia, Obesity, peripheral arterial disease, Family history.

Type of MI:

. Transmural infaction:

  • . Most common type.
  • . The artery is completely occlusive due to thrombus formation on disrupted plaque.
  • . Involves the whole thickness of the myocardium.
  • . All involves at least a portion of left ventricle.
  • . New Q waves develop in an ECG.
  • . ST segment elevation in ECG.

Subendocardial infaction:

  • . In this case the artery supply the area is not completely occlusive, though there is disruption of plaques with thrombus formation.
  • . Less common type.
  •  Involves the inner third of the myocardium.
  • . Emcompasses the entire perfusion zone of the occluded artery.
  • . Q waves are absent.

PATHOGENESIS Of MI (Heart Attack):

  • Sudden disruption of atheromatous plaque.
  • Subendocardial collagen and necrotic plaque contents are exposed.
  • Platelets adhere to the exposed material and undergo aggregation , activation and released potent aggregates( thromboxane A2 & platelets factor 3 and 4 ).
  • Platelets aggregation and release of mediators stimulate vasospasm.
  • Within minutes the thrombus evolves to completely occluded the lumen of coronary vessels.
  • Occlusion of the coronary vessels result in cessation of aerobic glycolysis and initiation of anaerobic glycolysis leading to:
  • Inadequate production of ATP.
  • Accumulation of toxic product ( lactic acid).
  • The predominant mechanism of cell death is coagulation necrosis.
  • myocardial infaraction

Biochemical changes:

  • Anaerobic glycolysis = second.
  • Loss of contractility = less than 2 min.
  • ATP reduces to 50% of normal = 10 min.
  • Irreversible cell injury = 20 – 40 min.
  • Micro- vascular cell injury = more than 1 hour.
  • Necrosis is complete = 6-12 hr.

Clinical features:

Chest pain;

  • Sudden onset of severe retrosternal chest pain lasting more than 30 – 45 minutes.
  • Pain is central and diffuse.
  • Pain is tight, squeezing and choking in character.
  • Pain is radiates to the left arm, jaw and neck.
  • Pain is aggravated by exertion and emotion.
  • Pain is not relived by nitroglycerine and rest.

Associated synptoms:

  • Breathlessness
  • Anxiety
  • Diaphoresis
  • Nausea and vomiting.

Cardiac enzyme in  (Heart Attack):

Elevated within Peak Return to normal
CK-MB 2-4 hr 24hr 72 hr
Troon in I & T 2-4 hr 28 hr 7-10 days
LDH 24 hr 3-6 days 8-14 days

 

Microscopic Morphology of MI:

  • Necrotic myocardium, acute inflammation ( 1- 3 days after MI ).
  • Wave of macrophages that remove necrotic myocardium ( 5- 10 days after MI ).
  • Formation of granulation tissue ( 1- 2 weeks after MI).
  • Scaring ( most advanced by the end of 6th week ).

Localization of MI:

Distribution of coronary artery thrombosis;

  • . Left anterior descending = 45%
  • . Right coronary artery = 35%
  • . Left circumflex coronary artery = 15%
  • ECG consist of Q waves, ST segment elevation, T- waves inversion.
  • Inverted T waves = area of ischemia at the periphery of the infarct.
  • Elevated ST segment = injured myocardial cells surrounding the area os necrosis.
  • New Q waves = area of coagulation necrosis.
  • ECG diagnosis of MI can localized the affect site.
Area of infarction ECG changes Artery involved
Inferior wall MI II, III, a VF Right coronary
Anteroseptal MI V1-V2 Left anterior descending
Anterolateral MI V4-V6 Left circumflex
Lateral wall MI I,ALL,  V5, V6 Left circumflex
Posterior V1-V4, ST segment, upright T waves Posterior descending

 

Complication of MI;

Arrhythmia:

. Heart rate less than 60.

. No cannon A waves.

Third degree heart block;

. Heart rate less than 60.

  • Contractile dysfunction.
  • Papillary muscle dysfunction.
  • Right ventricular infarction.
  • Myocardial rupture.
  • Chamber dilation.
  • Mural thrombus.
  • Ventricular Aneurysm.
  • Progressive late heart failure.

Treatment (DRUGS) Myocardial Infarction:

  • Aspirin.
  • Thrombolytics.
  • Antiplatelet agents.
  • Other blood-thinning medications.
  • Pain relievers.
  • Nitroglycerin.
  • Beta blockers.
  • ACE inhibitors.

Filed Under: Medicine Tagged With: Heart Attack, Myocardial infarction, Myocardial infarction notes, myocardial infarction pathology, myocardial infarction types

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