Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Ec gs in ami

ECGs in STEMI and NSTEMI
STEMI equivalents and STEMI mimic

  • Be the first to comment

Ec gs in ami

  1. 1. ECGs in AMI Kyaw Soe Win Department of Cardiovascular Medicine Mandalay General Hospital
  2. 2. Important to remember! •ECG is not sufficiently specific or sensitive to be used without a patient's clinical history
  3. 3. “Other cardiac” includes, among other, myocarditis, Tako-Tsubo cardiomyopathy, or tachyarrhythmias. “Non-cardiac” refers to thoracic diseases such as pneumonia or pneumothorax. . If the initial evaluation suggests aortic dissection or pulmonary embolism, D-dimers and MDCT angiography are recommended 2015 ESC Guideline for management ofACS
  4. 4. ECG changes in AMI ST Elevation MI non-ST Elevation MI
  5. 5. Acute Myocardial Infarction The leading symptom in patients with suspected AMI is chest pain. • Non-STEMI • No ST-elevation • Partially blocked artery • STEMI (STEMI) • ST-elevation myocardial infarction • Completely blocked artery • Critical need for quick reperfusion
  6. 6. Ischemic cascade
  7. 7. • When blood supply is abruptly reduced or cut off to a region of the heart, a sequence of injurious events occur with • Ischemia • injury • necrosis (infarction) • fibrosis (scarring) if the blood supply isn't restored in an appropriate period of time. • The ECG changes over time with each of these events… ST Elevation and non-ST Elevation MIs
  8. 8. ST depression ST elevation Q wave
  9. 9. Ways the ECG can change include: Appearance of pathologic Q-waves T-waves peaked flattened inverted ST elevation & depression ECG Changes in the MI
  10. 10. Ischaemic ECG changes Q wave Infarct Myocardial salvage possible No Myocardial salvage
  11. 11. ECG effects of myocardial injury ▪Deviation of the ST segment ▪ST segment deviated towards the surface of the injured tissue ▪Patterns of deviation ▪ST depression- transmural & epicardial ▪ST elevation- endocardial The position of the ST segment is commonly judged as normal or abnormal using the baseline of the PR or TP interval as a reference
  12. 12. TRANSMURAL Injury ST Elevation ECG Changes in the MI There are two distinct patterns of ECG change depending if the infarction is: Non-ST Elevation (Subendocardial or non-Q-wave) ST Elevation (Transmural or Q-wave),
  13. 13. ECG changes in myocardial ischemia • Manifest by changes in Ventricle repolarization (ST segment and T waves) ▪ST- isoelectric ▪T - same polarity with QRS Normal
  14. 14. ECG changes in myocardial ischemia • Manifest by changes in Ventricle repolarization (ST segment and T waves) ▪ST- isoelectric ▪T - same polarity with QRS • Imbalance between myocardial oxygen demand and supply • ST depression and/or T inversion Normal Ischaemia
  15. 15. Types & causes of ST depression • A – upward ➔ may be normal • B – down sloping ➔ strain / digoxin effect • C – planar ➔ ischaemia***▪Angina ▪NSTEMI ▪LVH ▪Digoxin effect Horizontal or downsloping ST depression ≥ 0.5 mm at the J-point in ≥ 2 contiguous leads indicates myocardial ischaemia.
  16. 16. T Wave • Deep and symmetrically inverted T waves may suggest cardiac ischemia • A T wave elevated more than half the height of the QRS complex (peaked T wave) may indicate a new onset of myocardial ischemia or hyperkalemia ▪At least 1 mm deep ▪Present in ≥ 2 continuous leads ▪Dynamic — not present on old ECG or changing over time
  17. 17. Widespread T wave inversion due to myocardial ischaemia Types of T wave changes in ischaemia
  18. 18. Point to note • Inverted T waves are normal in leads III, aVR, and V1 • Associated with a predominantly negative QRS complex. Other causes of T inversion A – T wave in coronary insufficiency B – T wave in LVH with strain C – T wave in digitalis effect
  19. 19. ST depression & T-wave inversion The ECG changes seen with a non-ST elevation infarction are: Before injury Normal ECG ST depression & T-wave inversion ST returns to baseline, but T-wave inversion persists Ischemia Infarction Fibrosis Non ST Elevation MI
  20. 20. ECG manifestations suggestive of acute NSTEMI ( in the absence of LVH and BBB) Fourth universaldefinition of myocardial infarction , EHJ (2018)00,1-33 ST depression T wave inversion Use Sgarbossa!
  21. 21. NSTEMI “subendocardialinfarct” ▪ Clinical spectrum of acute coronary syndrome ▪ sub-total occlusion of coronary vessel ▪ Current guideline emphasize risk stratification of UA/NSTEMI patients with respect to selecting a conservative versus an early invasive approach Ragavendra R. Baliga , MD , MaGraw-Hill Specialty Board Review , ISBN978-0-07-161410-8
  22. 22. Why ECG is clinically important in NSTEMI? ▪When ECG changes occur in association with chest pain but without frank infarction, they confer prognostic significance. ▪About 20% of patients with ST depression and 15% with T inversion will experience severe angina, myocardial infarction, or death within 12 months of their initial presentation.
  23. 23. Why ECG is clinically important in NSTEMI? • ST depression ≥ 2 mm in ≥ 3 leads is associated with a high probability of NSTEMI and predicts significant mortality (35% mortality at 30 days).
  24. 24. Management Early diagnosis Early treatment Time = myocardium STEMI .Life–threatening condition .Plaque rupture .Acute obstruction of infarct artery (s) Mortality is higher if a greater number of ECG leads show ST elevation
  25. 25. ST depression, peaked T-waves, then T-wave inversion The ECG changes seen with a ST elevation infarction are: Before injury Normal ECG ST elevation & appearance of Q-waves ST segments and T-waves return to normal, but Q-waves persist Ischemia Infarction Fibrosis ST elevation MI
  26. 26. ST elevation MI A. Normal ECG prior to MI C. Infarction from ongoing ischemia results in marked ST elevation B. Ischemia from coronary artery occlusion results in ST depression (not shown) and peaked T-waves D/E.Ongoing infarction with appearance of pathologic Q-waves and T-wave inversion F. Fibrosis (months later) with persistent Q- waves, but normal ST segment and T- waves
  27. 27. STEMI is a clinical syndrome defined by characteristic symptoms of myocardial ischemia in association with persistent (ECG) ST elevation and subsequent release of biomarkers of myocardial necrosis. STEMI Diagnosis
  28. 28. Criteria for diagnosing STEMI on ECG It is always impossible to identify STEMI without the 12 leads
  29. 29. • standard teaching for STEMI typically has the following criteria .≥1 mm (0.1 mV) of ST segment elevation in the limb leads .≥ 2 mm elevation in the precordial leads and present in anatomically contiguous leads There are several variations from the classic STEMI ECG changes that do not fit this definition Conventional STEMI
  30. 30. 2013 STEMI criteria Diagnostic ST elevation in the absence of left ventricular (LV) hypertrophy or left bundle-branch block (LBBB) is defined as new ST elevation at the J point in at least 2 contiguous leads of: In V2-3 ≥ 0.2mV in men ≥40 years ≥ 0.25mV in men <40 years ≥ 0.15mV in women In other leads ≥ 0.1mV for both sexes examples of ST-elevation in MI
  31. 31. 1.New or presumed new “Left Bundle Branch Block” in isolation is no longer an indication for a STEMI 2. Providers should use Sgarbossa’s Criteria to diagnose STEMI in the presence of LBBB 3. Isolated S-T depression in V1-4 is an indication of a posterior MI 4. Widespread S-T depression with S-T elevation in aVR is an indication of proximal LAD or LMCA occlusion. 5. Hyperacute T-waves without S-T elevation may be an early indicator of a STEMI 2013 changes in STEMI criteria
  32. 32. • The ECG is considered an essential part of the diagnosis and initial evaluation of patients with acute chest pain. • The information that can be obtained from the admission ECG in patients with STEMI • Various ECG patterns and the localisation of the infarct and the underlying coronary anatomy. • Reperfusion vs conservative & types of reperfusion • prediction of infarct size • estimation of prognosis Why ECG is important in STEMI
  33. 33. In transmural MI, ischemia in the subendocardium spreads to the epicardium and involves full thickness of the myocardium. In the acute phase, the ECG signs are ST segment elevation. ECG changes in infarction NSTEMI/ischaemia Transmural infarct: STEMI
  34. 34. STEMI?? Phase?? Site?? High Risk patient?? ST elevation !!!
  35. 35. Identify the J Point Junction Point or J Point
  36. 36. Don’t compare J Point to the PRI segment, there are medical conditions that my cause PRI depression Identify the J Point elevation
  37. 37. Identify the J Point elevation The TP segment provides the best baseline to evaluate ST elevation ▪ Locate the J-Point ▪ Compare it to the TP Segment ▪ Determine if the J point is elevated by 1mm or more above the TP Segment
  38. 38. ST segment morphology in other conditions Convexity upward infarction STEMI Mimic Concavity upward
  39. 39. Hours to days later during the evolving phase, pathological Q waves appear, the elevated ST segments return towards baseline, and the T waves become inverted. ECG changes in infarction Hyperacute T waves may precede ST segment elevation (A) or seen at the same time with ST elevation (B) during this acute phase. ST elevation The elevated ST segment may slope upward or be horizontal or dome-shaped.
  40. 40. Hyperacute T-waves Tall, narrow, symmetrically peaked T-waves are characteristically seen in hyperkalaemia. asymmetrically peaked or ‘hyperacute’ T-waves are seen in the early stages of ST-elevation MI (STEMI)
  41. 41. Q wave • Normal ✓Lateral leads (I,aVL,V5,V6) ✓III alone may be present Pathologic Q-waves ▪ ¼ of following R wave ▪ >0.04sec width(>1 mm) ▪ > One leadsNotice the small Normal Q Notice the deep & wide Infarction Q
  42. 42. Evolutionary changes( Phases) in STEMI • Tall T waves • ST elevation • Decrease of ST elevation with the beginning of Q wave & T waves inversion • Q wave, Isoelectric ST with symmetrical T wave inversion • Q wave, Isoelectric ST with upright T wave Hyper-acute Evolving Fully evolved Old Bayes de Luna ,The 12-lead ECG in ST elevation myocardial infraction , ISBN-13: 978-1-4051-5786-5 Minutes Hour(s) days Weeks/month
  43. 43. Anterior STEMI: Hyperacute
  44. 44. Anterior STEMI: evolving ST No Q/ no T inversion Benefit for reperfusion therapy
  45. 45. Anterior STEMI: evolving Benefit for reperfusion therapyST Q/ T inversion
  46. 46. Anterior STEMI: fully evolved QS ST T inversion No Benefit for reperfusion therapy
  47. 47. Old Anterior MI QS & upright T waves
  48. 48. Maximizing information from the ECG in acute MI •Which artery is blocked? •Where is the artery blocked? (extent of infarct) •Can one identify the high risk patient? •Large/ extensive infarct? •AV block? •VT/VF? •AF?
  49. 49. In order to recognize STEMI you have to know 2 things • What to look for (ST elevation) • Where you are looking (which Lead) STEMI-Location • Look in all leads for ST elevation except aVR • Is ST elevation present in 2 contagious leads? • Localize the STEMI based upon the leads showing the ST elevation • Area of infarction is reflected by the area of ST-Elevation • Reciprocal changes are NOT necessary to diagnose a STEMI. It needs to estimate time of STEMI (Phase)
  50. 50. Right Ventricle Left VentricleS Posterior Wall Lateral Wall Anterior WallV1 V2 V3 V4 V5 V6 Septum Anatomic Contiguous Leads
  51. 51. Arrangement of Leads on the ECG Limb leads chest leads
  52. 52. Anatomic Groups (Septum)
  53. 53. Anatomic Groups (Anterior Wall)
  54. 54. Anatomic Groups (Inferior Wall)
  55. 55. Anatomic Groups (Lateral Wall)
  56. 56. Anatomic Groups (Contiguous Leads)
  57. 57. Contiguous Leads extensive anterior V1 V2 V3 V4 V5 V6 I aVL II III aVF
  58. 58. I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 Left Ant Descending artery Anterior infarction Culprit vessel: LAD ST elevation V1 -4 I aVL,reciprocal ST depression in II III aVF
  59. 59. Anterior MI : anteroseptal ST-Elevation in leads V1 V2 V3 and V4 Culprit vessel: LAD
  60. 60. ST elevation V1 V2 V3 V4, reciprocal ST depression in II III aVF Anterior MI : anteroseptal Culprit vessel: LAD
  61. 61. I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 LADA ST elevation V1 V2 V3 I aVL, reciprocal ST depression in II III aVF Culprit vessel: LADAnterior MI : anterolateral
  62. 62. ST elevation V2 V3 V4 V5 V6 I aVL, reciprocal ST depression in II III aVF aVR Anterior MI : anterolateral Culprit vessel: LAD
  63. 63. I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 Left circumflex artery Lateral infarction Culprit vessel: LCX ST elevation V5 V6 I aVL, reciprocal ST depression in II III aVF
  64. 64. • Low Lateral AMI Lateral MI ST elevation V4 V5 V6 I aVL, reciprocal ST depression in III Culprit vessel: LCx
  65. 65. Inferior Infarction I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 Right coronary artery Culprit vessel: RCA ST elevation II III aVF
  66. 66. Inferior MI • ST-Elevation in leads II,III, and AVF • Reciprocal changes in leads I and AVL Culprit vessel: RCA
  67. 67. RCA vs LCx in Acute Inferior MI
  68. 68. Inferior Infarction Right coronary artery • ST elevation Lead III > Lead II • AV nodal block • ST-segment vector is directed toward the right (lead III). • ST-segment elevation in lead V1 -proximal occlusion of RCA with associated RVMI Left circumflex artery ▪ ST elevation Lead II > lead III ▪ ST-segment vector directed toward the left (lead II). ▪ There is an isoelectric or ST segment elevation in lead aVL Zimetbaum PJ, Josephson ME. Use of the electrocardiogram in acute myocardial infarction. N Engl J Med 2003;348:933-940
  69. 69. ST elevation withQ waves in the inferior leads with reciprocal changes in I and aVL ST elevation III > II Inferior MI Culprit vessel: RCA
  70. 70. Inferior MI Culprit vessel: LCX ST elevation in the inferior leads, I and aVL ST elevation II > III
  71. 71. Association of inferior wallMI ✓Heart block ( any degree ) ✓sinus node disease ✓Posterior wall MI ✓RV infarction ✓Mechanical complication ; acute mitral regurgitation
  72. 72. Posterior wall MI ▪Difficult to diagnose by Surface ECG ▪Posterior leads(V789) show ST elevation ▪Manifested by ST depression and upright T waves in V1 and V2( Just opposite to MI) Posterior MI accompanies 15-20% of STEMIs, usually occurring in the context of an inferior or lateral infarction.
  73. 73. V7-V9 = Posterior leads 2 52017 ESC Guidelines for the management of acute myocardial infarctionin patients presentingwith ST-segmentelevation Posterior wallSTEMI ( may or may not be associated with inferior wall MI)
  74. 74. 15 Lead ECG
  75. 75. Typical appearance of posterior infarction in V2 V2 V2 Mirror image of posterior infarction in V2
  76. 76. Posterior wall STEMI ( concomitant with inferior wall MI)
  77. 77. Posterior wall STEMI: isolated ( no concomitant with inferior wall MI)
  78. 78. Inferior MI with ST depression in anterior leads (ant ischaemia) vs inferior MI combined with posterior MI Anterior ischaemia
  79. 79. Posterior wallMI 2017 ESC Guidelines for the management of acute myocardial infarctionin patients presenting with ST-segmentelevation • Horizontal ST depression ≥0.5mm in posterior leads V7-9 • Horizontal ST depression ≥0.5mm • Tall R waves :R/S ratio > 1 in V2 V3 • Upright T waves Posterior MI: Tall R and Tall T with ST↓ in V1-V3
  80. 80. Right ventricularinfarction ▪ Usually associated with inf MI ▪ hypotension ▪ nitrates or diuretics may compound the hypotension ▪ may respond to fluid challenge FrancisMorris, ABC of clinicalelectrophysiology , BMJ book , ISBN 0 7279 15363 2017 ESC Guidelines for the management of acute myocardial infarctionin patients presenting with ST-segmentelevation V3R V4R lead
  81. 81. 2017 ESC Guidelines for the management of acute myocardial infarctionin patients presentingwithST-segmentelevation V3R V4R lead
  82. 82. The three ST-Segment and T-Wave configurations that an be identified by Lead V4R in patients with Acute Inferoposterior Myocardial Infarction. Wellens HJ. N Engl J Med 1999;340:381-383. RVMI ▪Right leads show ST segment elevation(V3R and V4R) ▪ST elevation in V1 in presence of IWMI, suspect RVMI ▪In presence of IWMI, ST elevation in lead III>II suspect RVMI
  83. 83. Right ventricular infarction ( concomitant with inferior wall MI) ST elevation in II , III and aVF andV1 ST elevation in V1 with inferior infarct indicates RVMI
  84. 84. Combination STEMI • Inferolateral+post AMI ST elevation II III aVF V5 V6, ST depression in v1–v4 aVR (post MI)Right coronary artery
  85. 85. The high risk patient • Age > 75 years • DM • Previous MI • Killip Class ¾ HF • Shock •Large MI: many leads •Sustained monomorphic VT •Late atrial fibrillation •AV blocks •VF Clinical ECG High mortality
  86. 86. ST elevation withQ waves in the inferior leads with reciprocal changes in I and aVL ▪ Diagnosis ; Acute inferior infarction with 2:1 AVblock
  87. 87. 3:2 AV block & 4:3 AV Block Anterior MI with AF
  88. 88. Ventricular fibrillation– complication ofSTEMI
  89. 89. Ventriculartachycardia ▪ Wide QRS complextachycardia Abnormal impulse from ventricular tissue No P wave beforeQRS complex Life – threatening condition ▪ Initial treatment ➢ Hemodynamic evaluation ✓ Stable hemodynamic ; antiarrhythmic drugs:amiodarone IV or lidocaine IV ✓ Unstable hemodynamic ; electrical cardioversion ✓ PulselessVT ; CPR withACLS and defibrillation
  90. 90. J A C C : Case Reports , V OL . 1 , NO . 4 , 2 0 1 9 Asatryan et al. December 2 0 1 9 : 6 6 6 – 8 ECG Equivalents of STEMI STEMI Equivalents
  91. 91. STEMI equivalents • Hyperacute T waves • De Winter ST T complex • Wellens T waves • Diffuse ST depression • Shark T • Sgarbossa Criteria • Posterior MI • New LBBB = No Longer STEMI Equivalents Use Sgarbossa!
  92. 92. • Hyperacute T waves • Tall , often asymmetrical, broad- based anterior T waves often associated with reciprocal ST depression • De Winter ST-T complex • ST segment depression at the J point with ascending ST segment and tall, asymmetrical T waves in the reciprocal leads, often combined with a 1-2mm elevation of ST segment in aVR • Wellens T waves • These ECG patterns are not always yet accompanied by chest pain and usually precede overt ST elevation myocardial infarction. They can be interpreted as an early sign of impending coronary occlusion ( with 24 hr) • Type A: deeply- inverted anterior T waves • Type B: biphasic anterior T waves
  93. 93. • Diffuse ST depression with ST elevation in aVR or V1 • aVR /V1= 0.1mV + 8 leads with ST depression = 0.1mV is moderately suggestive of left main coronary artery occlusion. • Shark T • J point depression transitioning in a convex ST segment • Sgarbossa Criteria • LBBB or pace maker rhythm with concordant or = 5mm ST elevation • Isolated Posterior MI • 0.05 mV ST depression in V1-3 especially associated with positive T waves (0.05 mV elevation in V7-9)
  94. 94. • The de Winter ECG pattern is an anterior STEMI equivalent that presents without obvious ST segment elevation. • Suggestive of proximal LAD lesion • Precordial ST-segment depression at the J-point • Tall, peaked, symmetric T waves in the precordial leads • aVR may shows slight ST elevation in most cases De Winter’s T wave N Engl J Med 2018;378:e22
  95. 95. De Winter’s T wave
  96. 96. De Winter’s T wave
  97. 97. N Engl J Med 2015;372:66 Wellens’ syndrome Critical stenosis of LAD Type A: Biphasic T-waves (initial positive deflection and terminal negative deflection) Type B: Deeply inverted and symmetric T-waves • ECG findings in absence of chest pain, but with recent cardiac chest pain symptoms • will require PCI in the next 24-48hr ( Widow maker syndrome)
  98. 98. Lawner et al. Cardiol Clin 2012; 30:591-99 Proximal LAD near-occlusion: Wellens syndrome One manifestation is the presence of biphasic T waves in the anterior precordial leads The commoner pattern is deep T-wave inversions in the anterior precordial leads
  99. 99. Isolated Posterior wallMI 2017 ESC Guidelines for the management of acute myocardial infarctionin patients presenting with ST-segmentelevation • Horizontal ST depression ≥0.5mm in posterior leads V7-9 • Horizontal ST depression ≥0.5mm • Tall R waves :R/S ratio > 1 in V2 V3 • Upright T waves RCA (90%), LCA (10%) Posterior MI: Tall R and Tall T with ST↓ in V1-V3
  100. 100. Isolated Posterior MI
  101. 101. • Seen with occlusion or near-occlusion of the left main artery or • Has been reported in occlusion of the proximal left anterior descending artery and severe multivessel coronary artery disease • 12-Lead ECG findings • ST depression is widespread and typically seen in lateral leads ( V4-6) • ST elevation in aVR ≥ 1mm • ST elevation in V1 ≥ 1mm Diffused ST depression
  102. 102. Diffused ST depression with ST elevation in aVR Left Main occlusion
  103. 103. Complete occlusion of the left main! After PTCA
  104. 104. ST elevation in aVR vs V1 •ST elevation aVR>V1: + ST depression in V4-6 • Left main 80% sensitivity and specificity •ST elevation V1>aVR :+ ST depression in V4-6 • Ostial/ proximal LAD Yamaji et al. JACC 2001; 38:1348-54
  105. 105. Proximal LAD occlusion Diffused ST depression with ST elevation in V1
  106. 106. 54y Male, Anterior MI on 11.6.2020 at MGH Primary PCI Ostial LAD
  107. 107. “Unfortunately, STE is a not an uncommon finding on the ECG of the chest pain patient; its cause infrequently involves AMI.” Brady et al., Electrocardiographic ST-segment elevation: correct identification of acute myocardial infarction (AMI) and non-AMI syndromes by emergency physicians (Acad Emerg Med 2001; 8(4):349-360) The Problem: Most STE is not MI
  108. 108. STEMI Mimic Beware of baseline ECG abnormalities (Artefacts) that may obscure interpretation ❖ Benign early repolarization ❖ Peri/myocarditis ❖ Brugada ❖ WPW syndrome ❖ Hyperkalemia ❖ LBBB ❖ LVH ❖ RBBB ❖ Cardiac pacing Sinus tachycardia
  109. 109. How common? • Retrospective review of ED charts over 3-month period • Looked at 902 adults with chief compliant of “chest pain” • Looked for STE in contiguous leads, >1mm limb leads, >2mm precordials • Compared final diagnoses, MI vs. other Brady et al., Cause of ST segment abnormality in ED chest pain patients (Am J Emerg Med 2001 Jan;19(1):25-8) Results Only 15% of STE patients had MI! 85% had non-MI diagnosis Sejersten et al. Comparison of the Ability of Paramedics With That of Cardiologists in Diagnosing ST-Segment Elevation Acute Myocardial Infarction in Patients With Acute Chest Pain (Am J Cardiol 2002 Nov 1;90(9):995-8) 51% false-positive rate Half of our diagnoses were wrong
  110. 110. ▪ Clinical correlation: Any suspicious ECG findings should be matched against patient presentation and physical exam. ▪ History and risk factors: Does hx supports MI – smoker, diabetic, hypertensive, aspirin use, etc? ▪ Old ECGs: Extremely valuable tool when available for establishing baseline. ▪ Serial ECGs: Repeat ECG may reveal dynamic changes with time/treatment. What are our tools for addressing this? But wait! ▪ No clinical sign/symptoms are completely reliable ▪ No ECG findings are completely reliable ▪ Hx regularly fools us The answer? You must look at the whole picture Diagnosis is based on a constellation of datapoints – not any one finding!
  111. 111. Computer interpretations Useless? Infallible? Neither! Just another tool. Depend on machine Bottom line: *** ACUTE MI SUSPECTED *** Not very sensitive But very specific Exactly what we need! Great tool for screening out false positives
  112. 112. Benign Early Repolarization Normal variant / J-point elevation most common STEMI mimic ▪ ST elevation focused in anterior (V2–V5) ▪ no reciprocal changes! ▪ no convex ST segments! ▪ no pathological Q waves! ▪ no acute evolution! ▪ no clinical signs/symptoms! ▪ almost always asso with well-developed R waves ▪ almost always asso with short QTc ▪ may have a notched J-point Smith et al. Electrocardiographic Differentiation of Early Repolarization From Subtle Anterior ST-Segment Elevation Myocardial Infarction. Ann Emerg Med. 2012 Jul;60(1):45-56.e2. Epub 2012 Apr 19
  113. 113. Benign Early Repolarization
  114. 114. Pericarditis •Diffuse, nonlocalized ST elevation, often in all leads except V1 and aVR (which will be depressed instead) •No reciprocal changes! •Widespread PR depression •Morphology resembles BER – generally modest STE that is concave, often notched, with substantial T waves
  115. 115. ECG inpericarditis ▪ Diffuse widespread ST/T elevation ▪ PR depression ( especially in lead II ) ▪ 4 stages of ECG finding Juan GuidoChiabrando, MD , Management of acute and recurrent pericarditis, JACC ,Vol 75, No 1 , 2020 Concavity upward ST elevation
  116. 116. Grasshopper -leg Brugada’s Syndrome
  117. 117. • Slurred initial entrance to QRS (“delta wave”) • Short PR (<120ms) • Wide or borderline wide QRS • Often resembles LVH and is confused with it • ST elevation generally discordant with QRS If diagnosis of WPW is clear, be skeptical about STEMI; symptoms are much more likely related to arrhythmia than to MI. Wolf-Parkinson- White Syndrome
  118. 118. Hyperkalemia • ECG findings that can resemble ACS • ECG presentation may correlate unreliably with level of serum K • History :Renal insufficiency is a major risk factor. medications and major soft tissue trauma (crush syndrome, burns) ECG findings: • Early sign is hyperacute T waves, which classically appear: • Symmetric, Narrow at the base and slim, With a “sharp” point • With a concave ST segment • Late sign: the QRS and T start to widen and merge, which both can cause apparent ST elevation (or depression if QRS is positive)
  119. 119. Serum K-7mmol/L Serum K-8mmol/L
  120. 120. Right Bundle Branch Block • In RBBB, the left bundle branch performs normally, activating the left side of the heart before the right • ECG characteristics – Initial negative deflection (S wave) – RSR-prime pattern – QRS (or in this case, RSR) duration at least 0.12 sec
  121. 121. Right Ventricular Hypertrophy ▪ Only notable differences from LVH: ▪ Generally most evident in V1–V3 ▪ Generally has right-axis deviation ▪ Presents similarly to posterior-wall MI with reciprocal changes, so keep an eye out Use Sgarbossa!
  122. 122. Left Bundle Branch Block • In LBBB, the fibers that usually fire the interventricular septum are blocked • ECG characteristics: – Initial Q wave in V1 – R wave in V1 – Deep, wide S wave (QS pattern) – QRS duration at least 0.12 sec
  123. 123. Left ventricular hypertrophy There is left axis deviation (positive in I, negative in II) and there are tall R waves in V5, V6 and deep S waves in V1, V2.
  124. 124. Ventricular Rhythms • Paced ventricular rhythms the only rhythm other than LBBB with empirical support for Sgarbossa’s criteria • Do people with pacemakers have heart attacks? . . . • Nothing new here – use the rules – follow serial ECGs – use your head Sgarbossa et al. Early Electrocardiographic Diagnosis of Acute Myocardial Infarction in the Presence of Ventricular Paced Rhythm. Am J Cardiol, 1996; 77: 423–424. Pacing spikesUse Sgarbossa!
  125. 125. Sgarbossa’s Criteria This principle applies to: • LBBB • RBBB • LVH (“strain pattern”) • Paced ventricular rhythms • Non-paced ventricular rhythms (including PVCs) • WPW and other preexcitation Even “new” LBBB is not an indicator of MI! new LBBB in the setting of AMI may be an indicator of high risk
  126. 126. Sgarbossa’s Criteria In the setting of chest pain and LBBB: • Concordant STE ≥1mm in any lead with a positive QRS (5p) • Concordant ST depression ≥1mm in V1, V2, or V3 (3p) • Discordant ST elevation ≥5mm in any lead with negative QRS (2p) Sum up the points: ≥3 is 98% specific for MI, 20% sensitive ≥2 is 61–100% specific, 20–79% sensitive Tabas et al. Electrocardiographic criteria for detecting acute myocardial infarction in patients with left bundle branch block: a meta-analysis. Ann Emerg Med. 2008 Oct;52(4):329-336.e1. Epub 2008 Mar 17. 5 points 3 points2 points
  127. 127. LBBB , no MI LBBB with anterior MI Sgarbossa score = 5 + 2
  128. 128. Left ventricular hypertrophy AMI with LVH ST elevation > 25% of QRS amplitude AND STE in 3 contiguous leads OR of T inversions in the anterior leads) is strongly suggestive of AMI
  129. 129. ▪not ↑ ST segment (T ↓ and ST↓ more common) ▪Like LBBB, morbidity + mortality may be very high when AMI is associated with RBBB ▪Use Sgarbossa 2017 ESC Guidelines for the management of acute myocardial infarctionin patients presentingwith ST-segmentelevation Right Bundle Branch Block with MI
  130. 130. Marked ST segment elevation and absent R waves in lead V1-V6 Notching of the upstroke of the QRS complex ( Cabrera ‘ s sign ) is noted in V4 Acute MI in pacerhythm Chou’s Electrocardiographyin clinical practice , ISBN : 978-1-4160-3774-3 Use Sgarbossa! Pacing spikes
  131. 131. • Identify J point • Identify J point elevation • Myocardial injury ST elevation ? • Localize the leads ( two or more contagious leads)? • What does the computer think ? • localize the site of occlusion • Identify Phase of STEMI ? Are there reciprocal changes ? • High risk patients ? Arrhythmias ? • Does the ECG support an alternate diagnosis ? diagnosis other than STEMI? • Repeat History & Exam • Obtain serial ECGs to guide or confirm diagnosis • an old ECG available ? Bringing it all together
  132. 132. • Identify J point • Identify J point elevation • Myocardial injury ST elevation ? • Localize the leads ( two or more contagious leads)? • What does the computer think ? • localize the site of occlusion • Identify Phase of STEMI ? Are there reciprocal changes ? • High risk patients ? Arrhythmias ? • Does the ECG support an alternate diagnosis ? diagnosis other than STEMI? • Repeat History & Exam • Obtain serial ECGs to guide or confirm diagnosis • an old ECG available ? Bringing it all together
  133. 133. • Identify J point • Identify J point elevation • Myocardial injury ST elevation ? • Localize the leads ( two or more contagious leads)? • Are there reciprocal changes ? • What does the computer think ? • localize the site of occlusion • Identify Phase of STEMI ? High risk patients ? Arrhythmias ? • Does the ECG support an alternate diagnosis ? diagnosis other than STEMI? • Repeat History & Exam • Obtain serial ECGs to guide or confirm diagnosis • an old ECG available ? Bringing it all together infarction
  134. 134. • Identify J point • Identify J point elevation • Myocardial injury ST elevation ? • Localize the leads ( two or more contagious leads)? • What does the computer think ? • localize the site of occlusion • Identify Phase of STEMI ? Are there reciprocal changes ? • High risk patients ? Arrhythmias ? • Does the ECG support an alternate diagnosis ? diagnosis other than STEMI? • Repeat History & Exam • Obtain serial ECGs to guide or confirm diagnosis • an old ECG available ? Bringing it all together
  135. 135. • Identify J point • Identify J point elevation • Myocardial injury ST elevation ? • Localize the leads ( two or more contagious leads)? • What does the computer think ? • localize the site of occlusion • Identify Phase of STEMI ? Are there reciprocal changes ? • High risk patients ? Arrhythmias ? • Does the ECG support an alternate diagnosis ? diagnosis other than STEMI? • Repeat History & Exam • Obtain serial ECGs to guide or confirm diagnosis • an old ECG available ? Bringing it all together
  136. 136. • Identify J point • Identify J point elevation • Myocardial injury ST elevation ? • Localize the leads ( two or more contagious leads)? • What does the computer think ? • localize the site of occlusion • Identify Phase of STEMI ? Are there reciprocal changes ? • High risk patients ? Arrhythmias ? • Does the ECG support an alternate diagnosis ? diagnosis other than STEMI? • Repeat History & Exam • Obtain serial ECGs to guide or confirm diagnosis • an old ECG available ? Bringing it all together
  137. 137. • Identify J point • Identify J point elevation • Myocardial injury ST elevation ? • Localize the leads ( two or more contagious leads)? • What does the computer think ? • localize the site of occlusion • Identify Phase of STEMI ? Are there reciprocal changes ? • High risk patients ? Arrhythmias ? • Does the ECG support an alternate diagnosis ? diagnosis other than STEMI? • Repeat History & Exam • Obtain serial ECGs to guide or confirm diagnosis • an old ECG available ? Bringing it all together
  138. 138. • Identify J point • Identify J point elevation • Myocardial injury ST elevation ? • Localize the leads ( two or more contagious leads)? • What does the computer think ? • localize the site of occlusion • Identify Phase of STEMI ? Are there reciprocal changes ? • High risk patients ? Arrhythmias ? • Does the ECG support an alternate diagnosis ? diagnosis other than STEMI? • Repeat History & Exam • Obtain serial ECGs to guide or confirm diagnosis • an old ECG available ? Bringing it all together
  139. 139. • Identify J point • Identify J point elevation • Myocardial injury ST elevation ? • Localize the leads ( two or more contagious leads)? • Are there reciprocal changes ? • What does the computer think ? • localize the site of occlusion • Identify Phase of STEMI ? High risk patients ? Arrhythmias ? • Does the ECG support an alternate diagnosis ? diagnosis other than STEMI? • Repeat History & Exam • Obtain serial ECGs to guide or confirm diagnosis • an old ECG available ? Bringing it all together
  140. 140. • Identify J point • Identify J point elevation • Myocardial injury ST elevation ? • Localize the leads ( two or more contagious leads)? • Are there reciprocal changes ? • What does the computer think ? • localize the site of occlusion • Identify Phase of STEMI ? High risk patients ? Arrhythmias ? • Does the ECG support an alternate diagnosis ? diagnosis other than STEMI? • Repeat History & Exam • Obtain serial ECGs to guide or confirm diagnosis • an old ECG available ? Bringing it all together infarction
  141. 141. thank you ▪ ECG is not sufficiently specific or sensitive to be used without a patient's clinical history ▪ You must look at the whole picture ▪ Diagnosis is based on a constellation of all data – not any one finding!

×