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Ecg in AMI


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Ecg in AMI

  1. 1. ECG in Acute Myocardial infarction & culprit artery localisation Dr.Nagaraj Moorthy SJIC 04-04-08
  2. 2. Introduction <ul><li>The ECG is considered an essential part of the diagnosis and initial evaluation of patients with chest pain. </li></ul><ul><li>The information that can be obtained from the admission ECG in patients with STEMI, </li></ul><ul><li>(1) prediction of infarct size, </li></ul><ul><li>(2) estimation of prognosis, and </li></ul><ul><li>(3) Various electrocardiographic patterns and the localisation of the infarct and the underlying coronary anatomy. </li></ul><ul><li>ECG without extra costs or time </li></ul>
  3. 3. Introduction <ul><li>The ECG remains a crucial tool in the identification and management of AMI. </li></ul><ul><li>A detailed analysis of patterns influence decisions regarding the use of reperfusion therapy. </li></ul><ul><li>Early and accurate identification of the IRA on the ECG can help predict the amount of myocardium at risk. </li></ul><ul><li>ECG signs of reperfusion represent an important marker of microvascular blood flow and consequent prognosis. </li></ul><ul><li>Crucial for identifying new conduction abnormalities and arrhythmias that influence both short- and long-term outcome. </li></ul>
  4. 7. ECG changes in AMI <ul><li>In the early stages of AMI the ECG may be normal </li></ul><ul><li><50% of patients with AMI have clear diagnostic changes on their first trace. </li></ul><ul><li>About 10% of patients with a proved acute myocardial infarction fail to develop ST segment elevation or depression. </li></ul><ul><li>In most cases, however, serial ECG’s show evolving changes that tend to follow well recognised patterns. </li></ul>
  5. 8. ECG manifestations of AMI <ul><li>ST Elevation: </li></ul><ul><li>New ST elevation at the J-point in two contiguous leads with the cut-off points: </li></ul><ul><li>≥ 0.2 mV in men </li></ul><ul><li>≥ 0.15 mV in women in leads V 2 -V 3 </li></ul><ul><li>and /or </li></ul><ul><li> ≥ 0.1 mV in other leads </li></ul><ul><li>sensitivity of 56% and a specificity of 94%. </li></ul><ul><li>The addition of multiple QRST variables (Q waves, ST depression, T wave inversion, bundle branch block, axes deviations, and LVH) increased specificity. </li></ul>
  6. 9. ECG changes associated with Prior MI <ul><li>Any Ǫ wave in leads V 2 -V 3 ≥0.02 s or QS complex in leads V 2 -V 3 </li></ul><ul><li>Ǫ wave ≥ 0.03 s and ≥ 0.1 mV deep or QS complex in leads I , II, aVL, aVF or V 4 – V 6 </li></ul><ul><li>in any two contiguous leads </li></ul><ul><li>R-wave ≥ 0.04 s in V 1 -V 2 & R/S ≥ 1 with a concordant positive T-wave in the absence of a conduction defect. </li></ul>
  7. 10. Re infarction by ECG <ul><li>ST elevation of ≥ 0.1 mV re-occurs in a </li></ul><ul><li>patient having a lesser degree of ST </li></ul><ul><li>elevation or new pathological </li></ul><ul><li>Q waves in at least two contiguous leads, </li></ul><ul><li>particularly when associated with ischemic </li></ul><ul><li>symptoms. </li></ul>
  8. 11. AMI-Early Hyperacute Phase <ul><li>Increased VAT </li></ul><ul><li> amplitude of R ware </li></ul><ul><li>Straightening of the normal upward concavity </li></ul><ul><li>ST – T merge not to separate </li></ul><ul><li>T remains upright,amplitude increases, widens </li></ul>
  9. 14. Hyperacute T waves
  10. 15. Grading of ischemia- Sclarrovsky Birnbaum
  11. 19. Reciprocal and Indicative Changes
  12. 21. Early repolarisation pattern
  13. 22. Pericarditis
  14. 23. L V aneurysm
  15. 24. Hypertrophic cardiomyopathy
  16. 25. Reciprocal ST segment depression
  17. 26. Chronic Stable MI
  18. 27. Resolution of changes in ST segment and T waves
  19. 28. RVMI
  20. 29. Posterior wall MI
  21. 30. Ischemia and Infarction <ul><li>ST segment depression </li></ul><ul><li>may identify ischemia but non-localizing </li></ul><ul><li>ST segment elevation </li></ul><ul><li>identifies epicardial injury – localizing </li></ul><ul><li>T wave inversion </li></ul><ul><li>not good for identifying ischemia (nonspecific) but highly localizing if injury present </li></ul><ul><li>Q waves </li></ul><ul><li>good for diagnosis of MI and highly localizing </li></ul>
  22. 31. Transmural and subendocardial MI Q-MI does not always correlate with transmural MI Non-Q-MI does not always correlate with subendocardial MI
  23. 32. Q-wave Myocardial Infarction (1) <ul><li>Genesis of Q wave </li></ul><ul><ul><li>Death cells => loss of electrical forces => redirection of electrical forces from that area, it occurs during initial 0.04-.06 sec of QRS => Q wave in leads overlying infarction </li></ul></ul><ul><ul><li>Small amount of death issue => reduce the magnitude of normal mean force => reduction of R wave voltage </li></ul></ul>
  24. 33. Sampling through electrically “ silent” area into the cavity. In the cavity, all initial wavefronts are directed away  Q wave Transmural Injury Q wave
  25. 34. Q-wave Myocardial Infarction (2) <ul><li>Q wave criteria: </li></ul><ul><ul><li>0.04 sec wide </li></ul></ul><ul><ul><li>25% of the height of R wave in a given lead </li></ul></ul><ul><li>Exceptions: </li></ul><ul><ul><li>Q wave is confined to lead III </li></ul></ul><ul><ul><li>Q wave is confined to lead aVL and there are no other ECG abnormalities </li></ul></ul>
  26. 36. Regions of the Myocardium Inferior II, III, aVF Lateral I, AVL, V5-V6 Anterior / Septal V1-V4
  27. 38. Posterior wall MI <ul><li>Difficult to diagnose by Surface ECG </li></ul><ul><li>Manifested by ST segment depression and upright T waves in V1 and V2 ( Just opposite to MI) </li></ul><ul><li>Posterior leads my show ST segment elevation </li></ul>
  28. 39. Posterior Myocardial Infarction recent or probably acute <ul><li>Initial R wave in V1 and V2 > 0.04 sec with: </li></ul><ul><ul><li>R>S and ST depression with upright T waves </li></ul></ul><ul><ul><li>usually in setting of acute inferior MI </li></ul></ul><ul><ul><li>RVH, WPW and RBBB interfere with diagnosis of posterior MI </li></ul></ul>
  29. 40. RVMI <ul><li>Right leads show ST segment elevation( V3 and V4) </li></ul><ul><li>ST elevation in V1 in presence of IWMI, suspect RVMI </li></ul><ul><li>ST segment elevation in V1 > V2 in AWMI, suspect RVMI </li></ul><ul><li>In presence of IWMI, ST elevation in lead III>II suspect RVMI </li></ul>
  30. 41. Localisation of culprit vessel in AMI
  31. 42. <ul><li>CAG identifies vessel anatomy whereas the ECG reflects the physiology of the myocardium during acute ischaemia. </li></ul><ul><li>It is possible to observe restored vessel patency upon angiography with ECG evidence of ongoing ischaemia due to “no-reflow”, reperfusion injury, or myocardial damage that has already developed before reperfusion occurs. </li></ul><ul><li>While CAG remains the “gold standard” for identifying the infarct related artery, the ECG remains the gold standard for identifying the presence and location of acute myocardial ischaemia. </li></ul>
  32. 43. Coronary Artery Circulation
  33. 44. Coronary Artery Circulation <ul><li>Right Coronary Artery </li></ul><ul><li>right atrium </li></ul><ul><li>right ventricle </li></ul><ul><li>inferior wall of left ventricle </li></ul><ul><li>posterior wall of left ventricle </li></ul><ul><li>1/3 interventricular septum </li></ul>
  34. 45. Coronary Artery Circulation <ul><li>Left Anterior Descending Artery </li></ul><ul><li>antero-lateral surface of left ventricle </li></ul><ul><li>2/3 interventricular septum </li></ul><ul><li>Circumflex Artery </li></ul><ul><li>left atrium </li></ul><ul><li>lateral surface of left ventricle </li></ul>
  35. 47. Lesions in LAD D1 S1 D1
  36. 48. Proximal LAD
  37. 49. Terminology <ul><li>Proximal LAD – origin to S1 </li></ul><ul><li>Mid LAD – S1- S2 </li></ul><ul><li>Distal LAD – Beyond S2 </li></ul>
  38. 54. Proximal LAD before S1 <ul><li>ST ↑ in lead aVR </li></ul><ul><li>Complete RBBB </li></ul><ul><li>ST ↑ in V1 > 2.5 mm </li></ul><ul><li>ST ↓ in V5 </li></ul><ul><li>ST ↓ in lead II, lead III > 1mm </li></ul><ul><li>ST ↓ in lead aVF > 2 mm </li></ul>
  39. 55. Proximal to D1
  40. 57. Proximal to D1 <ul><li>Lateral wall </li></ul><ul><li>Q in aVL </li></ul><ul><li>ST ↓ in lead II, lead III, lead aVF > 1mm </li></ul>
  41. 58. Distal LAD
  42. 59. Distal to D1 <ul><li>ST ↓ in aVL </li></ul><ul><li>Absence of ST ↓ in lead II, lead III ,aVF </li></ul>
  43. 63. Localisation in IWMI
  44. 64. Right coronary artery <ul><li>Lead 3 ST elevation > Lead 2 ST elevation </li></ul><ul><li>AV nodal block </li></ul><ul><li>ST-segment vector is directed toward the right (lead III). </li></ul><ul><li>ST-segment elevation in lead V1 -proximal occlusion of RCA with associated RVMI </li></ul>
  45. 65. Left circumflex artery <ul><li>Lead 2 ST elevation > lead 3 ST elevation </li></ul><ul><li>ST-segment vector directed toward the left (lead II). </li></ul><ul><li>There is an isoelectric or elevated ST segment in lead aVL </li></ul><ul><li>Zimetbaum PJ, Josephson ME. Use of the electrocardiogram in acute myocardial infarction. N Engl J Med 2003;348:933-940 </li></ul>
  46. 66. Value RV4
  47. 74. AMI with LBBB <ul><li>LBBB can obscure the electrocardiographic diagnosis of AMI. </li></ul>
  48. 75. LBBB with MI
  49. 77. Sgarbossa’s criteria <ul><li>Sgarbossa et al NEJM 1996, 334: 481 </li></ul><ul><li>Ecg diagnosis of evolving AMI in the presence of LBBB </li></ul>
  50. 80. LBBB with AMI
  51. 81. WELLEN’S SYNDROME <ul><li>Clinical UA with: </li></ul><ul><ul><li>Inverted or biphasic T-waves in V2 and V3 </li></ul></ul><ul><ul><li>T wave changes may also be present in V1, V4-V6 </li></ul></ul><ul><ul><li>Changes appear when pain free </li></ul></ul><ul><ul><li>Little to no ST change </li></ul></ul><ul><ul><li>No loss of precordial R waves </li></ul></ul><ul><ul><li>No pathologic Q waves </li></ul></ul><ul><li>Concern: </li></ul><ul><ul><li>Highly specific for LAD lesions </li></ul></ul><ul><ul><li>At risk for extensive AMI or sudden death </li></ul></ul>
  54. 84. ? RVMI
  55. 85. ?RVMI
  56. 86. Localisation of culprit vessel <ul><li>Identification of the IRA is excellent </li></ul><ul><li>The specificity of the ECG in AMI is limited </li></ul><ul><li>by large individual variations in coronary anatomy </li></ul><ul><li>by the presence of preexisting coronary artery disease, </li></ul><ul><li>collateral circulation, </li></ul><ul><li>previous CABG.LBBB,Pre-exitation,V pacing </li></ul><ul><li>The ECG is also limited by its inadequate representation of the posterior, lateral, and apical walls of the left ventricle. </li></ul>
  57. 87. FACTORS THAT DETERMINE PROGNOSIS IN ACUTE MYOCARDIAL INFARCTION <ul><li>The immediate prognosis in patients with AMI is inversely related to the amount of myocardial reserves.(ischaemic area at risk), </li></ul>
  58. 89. ESTIMATION OF THE SIZE OF THE ISCHAEMIC MYOCARDIUM AT RISK <ul><li>ST elevation score </li></ul><ul><li>Sclarovsky-Birnbaum </li></ul><ul><li>Aldrich score: </li></ul><ul><li>% of myocardium at risk=3[0.6(# ST elevation II,III,aVF)+2] </li></ul><ul><li>% of myocardium at risk=3[1.5(#leads with of ST elevation)-0.4] </li></ul>
  59. 90. ESTIMATION OF THE SIZE OF THE ISCHAEMIC MYOCARDIUM AT RISK <ul><li>2D echo,ventriculography </li></ul><ul><li>ECG: </li></ul><ul><li>Aldrich et al studied patients with AMI who did not receive thrombolytic therapy.The best correlation between the final ECG Selvester QRS scoring system(an estimation of infarct size) and the admission ECG was found using the magnitude of ST elevation in leads II, III, and aVF in IWMI and the number of leads with ST elevation in AWMI. </li></ul><ul><li>However,in patients who received reperfusion therapy there was only week correlation between the Aldrich score and either the ischaemic area at risk or final infarct size, as measured by pretreatment and predischarge technetium 99m (99mTc) sestamibi </li></ul><ul><li>Clemmensen et al reported a good correlationbetween the final Selvester score and the number of leads with ST elevation ( r =0.70) in anterior myocardial infarction. </li></ul>
  60. 91. <ul><li>Clements et al also reported only a weak correlation between myocardial area at risk (as assessed by 99mTc sestamibi scan) and either the number of leads with ST deviation, total ST deviation, total ST elevation, or total ST depression.The myocardial area at risk correlated modestly ( r =0.58) with total ST deviation in anterior myocardial infarction, and with total ST depression normalised to the R wave ( r =0.70) in inferior myocardial infarction. </li></ul>
  61. 92. <ul><li>Limitations : </li></ul><ul><li>12-lead ECG does not equally represent all myocardial regions. </li></ul><ul><li>Ischaemia in opposed regions may attenuate or augment ST deviation </li></ul><ul><li>Many variables such as width of the chest wall, the distance of the electrode from the ischaemic zone, the myocardial mass, and presence of “ischaemic preconditioning” and collateral circulation have a major influence. </li></ul>
  62. 93. ECG Predictors of Reperfusion <ul><li>The presence of normal epicardial blood flow does not always correlate with microvascular perfusion of the myocardial tissue. </li></ul><ul><li>The absence of tissue perfusion is the most potent predictor of impaired ventricular function and the risk of death after myocardial infarction. </li></ul><ul><li>Resolution of ST-segment elevation-excellent marker of reperfusion, </li></ul><ul><li>ST-segment resolution is also useful for guiding reperfusion therapy. </li></ul><ul><li>A reduction in ST-segment elevation by more than 70 percent in the leads with maximal elevation is associated with the most favorable outcomes. </li></ul>
  63. 94. <ul><li>Other ECG markers of reperfusion include T-wave inversion within four hours after myocardial infarction. </li></ul><ul><li>An accelerated idioventricular rhythm is a highly specific marker of reperfusion. </li></ul><ul><li>This rhythm is benign and should not be suppressed with medication. Isolated ventricular premature depolarizations may also be seen with reperfusion. </li></ul><ul><li>Polymorphic VT and VF may be seen with reperfusion but are rare and should raise the suspicion of ongoing arterial occlusion. </li></ul>
  64. 95. Arrhythmias and Conduction Disease in AMI <ul><li>Conduction abnormalities AMI associated with a poor prognosis </li></ul>
  65. 97. Inferior Myocardial Infarction <ul><li>Can occur immediately or hours or days after MI Sinus bradycardia or varying degrees of atrioventricular block including CHB can occur within the first two hours after an AIWMI as a result of heightened vagal tone. </li></ul><ul><li>The AVN is the site of conduction disturbances in AIWMI </li></ul><ul><li>CHB is generally associated with a narrow complex escape rhythm of between 40 and 60 beats per minute . </li></ul><ul><li>Usually asymptomatic but may be associated with hemodynamic instability due to loss of atrioventricular synchrony. </li></ul><ul><li>Generally transient and resolves within five to seven days but may persist for up to two weeks. </li></ul>
  66. 98. Anterior Myocardial Infarction <ul><li>Due to necrosis of the intramyocardial conduction system. </li></ul><ul><li>Occurs almost exclusively in the presence of proximal occlusion of the LAD and septal necrosis. </li></ul><ul><li>Second-degree atrioventricular block with AWMI is usually Mobitz type II block secondary to block in the His–Purkinje system. </li></ul><ul><li>CHB results from extensive necrosis of the IVS. It usually occurs abruptly during the first 24 hours after myocardial infarction. </li></ul>
  67. 99. <ul><li>The development of bifascicular block with anteroseptal infarction is associated with as much as a 30 percent excess risk of complete heart block. </li></ul><ul><li>The mortality associated with CHB in AWMI, with or without preceding right bundle-branch block and left fascicular block, may be as high as 80 percent. </li></ul>
  68. 100. Post MI Risk Stratification Role of Electrocardiogram
  69. 101. At The Time of Presentation <ul><li>Predictors of size of MI </li></ul><ul><ul><li>Presence of Q waves with ST elevation </li></ul></ul><ul><ul><li>Number of leads with ST Elevation </li></ul></ul><ul><ul><li>Sum of ST Elevation in 12 leads </li></ul></ul><ul><ul><li>ST elevation in V4 with Inferior MI </li></ul></ul><ul><ul><li>Abnormal R in V1 (R/S>1) with inferior MI </li></ul></ul><ul><ul><li>Conduction disturbances </li></ul></ul><ul><li>Predictors of in hospital mortality </li></ul><ul><ul><li>Anterior location of MI </li></ul></ul><ul><ul><li>ST elevation in anterior and inferior leads </li></ul></ul><ul><ul><li>Evidence of earlier remote MI </li></ul></ul><ul><ul><li>Marked ventricular ectopic activity </li></ul></ul>
  70. 102. Risk Stratification after MI by ECG <ul><li>Presence of Q waves </li></ul><ul><li>ST Elevation in multiple leads </li></ul><ul><li>Persistent elevation of ST segment </li></ul><ul><li>Recurrent elevation of ST segment </li></ul><ul><li>RV infarct in Inf MI </li></ul><ul><li>Conduction disturbances </li></ul><ul><ul><li>AV blocks </li></ul></ul><ul><ul><li>Fascicular blocks </li></ul></ul><ul><ul><li>QRS duration </li></ul></ul><ul><li>Primary arrhythmias </li></ul><ul><li>Secondary arrhythmias </li></ul>
  71. 103. Conclusion <ul><li>12 lead ECG is of great value in Diagnosis of AMI </li></ul><ul><li>Site of occlusion of culprit artery </li></ul><ul><li>Decision regarding reperfusion </li></ul><ul><li>Recognising reperfusion </li></ul><ul><li>Recognising RV involvement </li></ul><ul><li>Identify risk of conduction block </li></ul><ul><li>Risk stratification </li></ul>
  72. 104. References : <ul><li>Braunwald’s heart disease,8 th Edn </li></ul><ul><li>The heart,hurst’s </li></ul><ul><li>Leo Schamroth,an introduction to electrocardiography,7 th Edn </li></ul><ul><li>SS Barold,Advanced 12 lead electrocardiogram,cardiology clinics.2006:24 </li></ul><ul><li>Robert roberts,prognosis after myocardial infarction,cardiology clinics.1984:2 </li></ul><ul><li>SS Barold,Advanced 12 lead electrocardiogram,cardiology clinics.1987:5 </li></ul><ul><li>Francis Morris, William J Brady, ABC of clinical electrocardiography </li></ul><ul><li>Acute myocardial infarction—Part I, BMJ VOLUME 324 6 APRIL 2002 </li></ul><ul><li>Peter J. Zimetbaum, Mark E. Josephson, Use of the Electrocardiogram in Acute Myocardial Infarction.nejm,2003: 348:933-940 </li></ul><ul><li>………………………………………………………………………… . </li></ul><ul><li>;…………………………………………………………………. </li></ul>
  73. 105. THANK YOU