STEMI stands for "ST-segment elevation myocardial infarction.''
Based on the ECG findings, myocardial infarctions are divided into two types.
STEMI, in which the ST segment of ECG elevates more than 1mm from the base line of ECG.Non-STEMI in which the ST segment don't elevate.
STEMI, Non-STEMI and Unstable angina are combinely called acute coronary syndrome (ACS).
We recommend you to read our article on basic of ECG so that you understand the ECG findings very well. Pathology in STEMI:
The pathophysiology of STEMI is that a coronary vessel is completely occluded by a thrombus. This results in the reduced blood supply or ischemia in the myocardium and if prolonged, may cause cardiac muscle death called myocardial infarction. The ST segment elevation shows acute injury to the myocardium of the heart due to ischemia. As the time passes, the muscle cells dies and the ST segments starts coming back to the baseline while q-wave amplitude increases. As soon as, the q-wave amplitude grows beyond 1/3 rd of the whole QRS complex, it becomes significant, and is called significant Q-wave denoted by capital letter "Q". The development of significant Q waves and the return of ST segment to the baseline show that the myocardial muscles have been completely died or myocardial infarction has occurred.
Clinical presentation of STEMI:All acute coronary syndromes (Unstable angina, STEMI, NSTEMI) present with severe chest pain, shortness of breath, profuse sweating, and irritability. The patient often looks too pale and will be so much irritable that even unable to talk to you. The chest pain is due to the ischemia of the myocardium. Chest pain due to unstable angina or NSTEMI usually comes with activity and relieves with rest but chest pain of STEMI usually comes at rest and don't relieve. This often is described as an "elephant setting on my chest" or the patient may have tightly grabbed his left chest or may have placed a clenched fist over his chest, called the Levine sign.
The pain often radiates to the left arm, neck and jaw. A patient with pain like this, when come, should be asked about the risk factors like smoking, dyslipidemias, hypertension, diabetes, previous cardiovascular diseases, valvular diseases etc. This will support you towards making a confident diagnoses. The pain may also radiate to the interscapular region but that signifies aortic dissection more than STEMI. If the patient can localize the pain with one finger it is less likely ischemic pain because ischemic pain involves a large area.
Remember:
Acute coronary syndromes, i.e unstable angina, NSTEMI, and STEMI, may present with epigastric pain too, if the inferior wall of the heart is involved. This is often mis-diagnosed with gastritis or GERD. So it is mandatory to order an ECG if a patient comes with severe epigastric pain and have positive risk factors for MI.
Silent MI:Silent MI is the myocardial infarction that don't present with pain. The patient may even be unaware of the fact that he has got MI. This is in case of autonomic neuropathy due to Diabetes Mellitus. The diagnoses is often missed because of the lack of experience and because of the lack of proper history. The patient may come only with the complaint of shortness of breath however if history suggest Diabetes Mellitus, an ECG should be ordered in which the ST elevation will show that silent MI has been occurred.
Diagnosis of STEMI:A patient presenting with the previously discussed features should be ordered ECG. If the ECG shows ST elevation of more than 1 mm with or without newly developed left bundle branch block (LBBB) ("W" or "M" pattern of QRS complex in V 5 and V 6 leads) or right bundle branch block (RBBB) ("W" or "M" pattern of QRS complex in V 1 and V 2 leads.), then this is STEMI. The serum levels of cardiac biomarkers i.e Troponins, and CK-MB etc are raised due to cellular injury.
An ST-segment depression or T-wave inversion shows ischemia or angina. The cardiac biomarkers are not raised in the serum in angina.
In case, ST-segment is neither elevated nor depressed in the ECG and there are no other findings in the ECG for ischemia, but the patient have chest pain then cardiac biomarkers in the serum should be checked. If serum level of biomarkers are raised then it is Non-STEMI or NSTEMI.
Causes of STEMI:Beta adrenergic stimulation in early morning cause increased vascular tone which lead to ischemia. Hypercoagulability and platelet hyperactivity may cause clot formation which may lead to thrombus formation and embolization. Thus history about the hypercoagulability states must be taken.
Sometimes an atherosclerotic plaque ruptures which lead to thrombus formation which cause complete obstruction of the vessel leading to infarction of the area supplied by that vessel.
Vigorous physical exercises, emotional stress and other illnesses may cause plaque disruption and thrombosis.
Localization of STEMI:First we recommend to learn the basis of normal EKG so that one can easily understand what we are trying to make you understand.
The myocardial area that is necrosed or injured due to ischemia can be localized from the group of ECG leads in which there is ST-segment elevation.
If the ST-segment is elevated in lead-I, avL, V 5 and V 6, this is called lateral wall STEMI. Reciprocal ST-segment depression may be observed in V 1 and V 2.
If the ST-segment is elevated in lead-II, III and avF, this is called inferior wall STEMI and this may present with epigastric pain.
If the ST-segment is elevated in V 3 and V 4 then it is called anterior wall STEMI.
If there are ST-depression in lead V 1 -lead V 4, then it may be posterior wall STEMI. In such case two more leads are planted on the back which will show ST-segment elevation.
Management options:The management of the acute STEMI include:
Pain control. (Pain control and sedation, both are given with morphins.) Anti-platelet therapy with Aspirin. Rapid vasodilation with sub-lingual nitroglycerin. IV beta blockers to inhibit adrenergic stimulation. Oxygen inhalation to improve oxygenation.
The patient is then assessed for re-perfusion therapies. If the ECG, cardiac biomarkers and clinical conditions suggest that necrosis still has not occurred, reperfusion therapy should be given that will save the myocardial cells from death but if necrosis has occurred there is no need.
The following options are available in re-perfusion therapies:
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