ST segment elevation myocardial infarction

The myocardial infarction with ST segment elevation of the is a medical emergency caused by the formation of a thrombus on a broken plate arteriosclerosis occluding the coronary circulation of the heart muscle . As a consequence, prolonged ischemia and necrosis of myocardial cells occur . It represents 36% of the cases admitted with the diagnostic suspicion of acute coronary syndrome , accompanied by a mortality of 6-10%.

Summary

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  • 1 Treatment
    • 1 Antiplatelet treatment
    • 2 Anticoagulant treatment
    • 3 Antianginal treatment
  • 2 References

Treatment

  • The goals of treating patients with ST-segment elevation myocardial infarction are the relief of ischemic pain, oxygen therapy when saturation is <90%, recognition and treatment of other complications such as hypotension by expansion of blood volume, pulmonary edema and disorders of the heart rate , as well as identification of candidates for reperfusion therapy. [one]
  • The fibrinolysis is the most frequently used treatment (30% to 70%) in the world in patients with myocardial infarction with ST segment elevation of the mainly due to operating difficulties for Angioplasty primary. [two]

Antiplatelet treatment

  • ST segment elevation myocardial infarction achieves improvement with antiplatelet agents. The aspirin , administered between 50-325 mg daily, and clopidogrel (75 mg daily) are recommended first – line options.
  • The aspirin causes irreversible inhibition of the activity of cyclooxygenase that in the plate , prevents the formation of thromboxane A2 , a potent agonist platelet
  • Clopidogrel selectively inhibits the P2Y 12receptor , which is one of the platelet receptors for adenosine diphosphate (ADP) , resulting in an increase in cyclic adenosine monophosphate (cAMP). These high cAMP values ​​cause a platelet refractory state by inhibiting platelet aggregation. In infarction, a loading dose of 300 to 600 mg is usually administered, followed by daily doses of 75 mg.

Anticoagulant treatment

  • The streptokinase (SK) combined with proactivator plasminogen and catalyzes the conversion of the plasminogen to plasmin . Plasmin is produced in the blood in order to break down the main components of blood clots and fibrin. SK, being a non-specific fibrinolytic, not only activates the plasminogen bound to fibrin but also the plasma, inducing an increase in the circulating concentration of plasmin. It also causes depletion of circulating fibrinogen and coagulation factors V and VIII.. In myocardial infarction, an initial bolus dose of 250,000 units is administered, followed by a maintenance dose of 100,000 units every hour for 24 hours.

Anti-anginal treatment

  • The nitroglycerin cause increased oxygen supply and demand decrease in the myocardium. It reduces coronary vascular resistance, increases collateral flow and improves perfusion of the endocardium, reducing blood pressure . Nitroglycerin is administered at sublingual 0.4mg every 5 minutes up to a maximum of 3 doses or before relief of symptoms is obtained.
  • The metoprolol is a cardioselective beta – blocker which acts on receptors beta1 located primarily in the heart. Metoprolol decreases or inhibits the stimulatory effect of catecholamines on the heart, leading to a reduction in heart rate, cardiac contractility, and cardiac volume-minute. The starting dose of metoprolol is 5 mg as intravenous therapy every 5 minutes for 3 doses and if the patient tolerates orally, 25-30 mg every 6-12 hours.
  • The Atropine (0.5 mg IV) and related compounds, compete with acetylcholine and other agonists muscarinic by a common binding site on the muscarinic receptor.
  • The Morphine produces analgesia appropriate by lowering the concentration of circulating catecholamines and reduces myocardial oxygen consumption. Morphine also produces venodilation, which decreases the preload of the heart, arterial vasodilation, and has a vagotonic effect that lowers the heart rate . Morphine is administered 2-4 mg IV every 5 minutes or until pain subsides
  • The digoxin binds to the extracellular binding site of the α subunit of the sodium-potassium pump in the cell membrane of myocytes or cardiac muscle fibers. This produces an increase in the entry of sodium into the cell, contributing to an increase in the concentration of calcium ions. The increase in intracellular calcium is stored in the sarcoplasmic reticulum and is released with each action potential, an effect that does not change with digoxin, therefore, at the same time, an increase in the contractility of the heart occurs. Start with a saturation dose of 0.25mg to 1mg in 24 hours and then a maintenance dose of 0.25mg orally.

 

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