AMI progression in terms of ECG changes - Essay Example

? AMI progression in terms of ECG changes of the Health sciences and medicine of the July 20. Discuss 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. AMI progression in terms of ECG changes Introduction ECG is recommended as the first diagnostic test that should be performed in a patient with suspected acute myocardial infarction (AMI) (O'Connor et al, 2010). 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 flows away from positive electrode. When depolarisation occurs, due to depressed baseline, ST segment becomes elevated. ST depression may occur with lesser degree of ischemia, limited to the subendocardium,. ST vector shifts towards ventricular cavity and ST depression is present in the leads overlying the ischemic myocardium ( Goldberger, 2001). The contribution of ATP sensitive potassium channels to ST depression is not clear (Herring & Paterson, 2006). ECG may show pseudoinfarct pattern of ST elevation simulating ischemia in conditions like acute pericarditis or a normal ‘early repolarisation’ pattern (Goldberger, 2001). Abnormal Q waves Changes in depolarisation (QRS complex) also occur during infarction. Myocardial necrosis leads to decreased amplitude of R waves or pathological Q waves (Goldberger, 2001). Their presence suggests absence of electrical activity as in complete infarction. Q waves are characteristically wider and broader than the normal q waves, present in anterior or inferior leads and remain permanently after a MI (Herring & Paterson, 2006). All Q waves in lead V1 to V3 are pathological. Also, Q waves more than 0.03 seconds in other leads points towards an established MI (Herring & Paterson, 2006). Posterior or lateral infarction may be associated a reciprocal increase in the amplitude of R waves in leads V1 and V2 with absent Q waves (Goldberger, 2001). T wave inversion Opening of ATP sensitive potassium channels in ischemic cells also shortens action potential duration reversing the gradient of repolarisation from epicardium to endocardium. This reversal leads to inversion of T wave over the next few hours (Herring & Paterson, 2006). T wave inversion may be transient or they may remain permanently inverted. The degree of T wave inversion has been shown to correlate with the extent of infarction (Bosimini et al, 2000) Presence of deep T wave inversion in multiple precordial leads is associated with severe occlusion of the left anterior descending (LAD) coronary artery. Some patients having acute transmural ischemia with pre-existing deep T wave inversions in their baseline ECG develop normalisation of T waves. This phenomenon is called pseudonormalization (Goldberger, 2001). Differential diagnosis of T wave inversion includes ventricular hypertrophy, cardiomyopathy and subarachnoid haemorrhage. Normalisation of the ST segment ST segment usually returns to normal as the infarct area progresses from necrosis to scar tissue (Herring & Paterson, 2006). Persistence of ST segment elevation after few weeks of a Q wave infarct is associated with high risk of an underlying wall motion disorder (Goldberger, 2001). Conclusion ECG changes evolve with the progression of AMI and are an important clue towards the current and pre-existing coronary artery disease. Diagnosing AMI changes on ECG is a fundamental skill for every health care provider, especially those working in pre-hospital and emergency settings. References Bosimini, E., Giannuzzi, P., Temporelli, P. L., Gentile, F., Lucci, D., Maggioni, A. P., et al. (2000).Electrocardiographic evolutionary changes and left ventricular remodelling after acute myocardial infarction: results of the GISSI-3 ECHO substudy. Journal of the American College of Cardiology, 35(1), 127-135. Retrieved from http://content.onlinejacc.org/data/Journals/JAC/22910/04878.pdf Goldberger, A. L. (2001). Electrocardiography. In E. Braunwald, A. S. Fauci, D. L. Kasper, S. L. Hauser, D. L. Longo & J. L. Jameson (Eds.), Harrison’s Principles of Internal Medicine (pp 1267-1269). India: McGraw Hill. Herring, N., & Paterson, D. J. (2006). ECG diagnosis of acute ischaemia and infarction: past, present and future. Quarterly Journal of Medicine, 99, 219–230. doi:10.1093/qjmed/hcl025 Houghton, A. R., & Gray, D. (2008). Making sense of the ECG (3rd ed.). London: Hodder Arnold. Nable, J. V., & Brady, W. (2008). The evolution of electrocardiographic changes in ST segment elevation myocardial infarction. American Journal of Emergency Medicine, 27, 734–746. doi:10.1016/j.ajem.2008.05.025 O'Connor, R. E., Brady, W., Brooks, S. C., Diercks, D., Egan, J., Ghaemmaghami, C., et al. (2010). Part 10: Acute Coronary Syndromes : 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation, 122, S787-S817. doi: 10.1161/CIRCULATIONAHA.110.971028 Sgarbossa, E. B., Birnbaum, Y., & Parrillo, J. E. (2001). 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