AMI progression in terms of ECG changes. How does each change reflect depolarisation movement in the affected myocardium? Your answer needs to specifically address ion movements during the action potential…
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It is immediately available, inexpensive and easy to perform. Also, it can point towards the region of myocardium (anterior, lateral, inferior, posterior) that has suffered the ischemic insult and help the clinician in detecting a recent ischemic coronary event as well as an old infarct (Sgarbossa, Birnbaum & Parrillo, 2001). This paper will describe the ECG changes that occur with the progression of AMI and specifically address ion movements during the action potential. AMI and ECG AMI can be classified in to two groups on the basis of changes in ECG. Myocardial infarction (MI) that is associated with elevation of the ST segment is called ST segment elevation myocardial infarction (STEMI). The other group is non-ST segment elevation MI (NSTEMI). This classification is important because the treatment protocols of AMI like immediate reperfusion therapy for STEMI are now based on the differentiation of AMI in to these two groups (O'Connor et al, 2010). Lack of transmural infarction is believed to be the cause of absence of ST elevation and Q waves in NSTEMI. AMI can also present with a new onset left bundle branch block. It should be kept in mind that AMI can occur without any change in the ECG (Houghton & Gray, 2008). In complete ischemia, there is cell death and no electrical activity. In less severe ischemia, hypoxia causes ATP dependent sodium potassium exchange pump to stall. This results in depolarisation because of loss of normal hyperpolarising currents and decreased intracellular and increased extracellular potassium concentration. Depolarisation also inhibits fast sodium channels and velocity of action potential upstroke and conduction velocity is decreased. ECG changes in acute myocardial infarction Rapidly after coronary artery occlusion leading to myocardial infarction (MI), ECG changes appear. Electrostatic properties of myocardial cells are affected by ischemia in time dependant fashion (Goldberger, 2001). Classically, in a ST- segment elevation MI (STEMI), these changes progress from tall hyperacute T waves and ST segment elevation to abnormal Q waves, inversion of T waves concluding with normalisation of ST segment (Nable & Brady, 2008). Usually, some abnormality in the ECG persists after STEMI. It may be abnormal/pathological Q wave or an inverted T wave (Houghton & Gray, 2008). These ECG changes reflect the changes in the electrical vectors of depolarisation and repolarisation in infracted myocardium as compared to the normal myocardium (Nable & Brady, 2008). Hyperacute T waves T waves become tall and ‘hyperacute’ within minutes of infarction. T wave changes may occur with or precede ST segment elevation (Houghton & Gray, 2008). Literature mentions that evolution of T wave changes after MI are because of a prolonged action potential in the myocardium adjacent to necrotic area (Bosimini et al, 2010). ST segment elevation Elevation of ST segment is measured as compared to the end of PR segment. The proposed mechanism for this elevation is injury currents between the infracted and normal myocardium. These currents are generated because of local areas of hyperkalemia resulting from open ATP sensitive potassium channels in the hypoxic cells (Herring & Paterson, 2006). In transmural ischemia, ST vector shifts towards the epicardium producing ST elevation and the above mentioned hyperacute T waves (Goldberger, 2001). Normal myocardium is repolarised and ischemic muscle cells are depolarised. Baseline voltage is depressed because electrical current
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