12 lead-lesson 5

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  • In this lesson, we are going to perform the third and fourth steps of the six step method.
  • In this lesson, we will learn a few more pathologies which can be identified on a 12-lead ECG. All of these conditions listed can be identified by examining the intervals and morphologies. Lets learn how.
  • When looking for ST-elevation that indicates an MI, we look for changes in contiguous or associated leads. Contiguous leads look at the same area of the heart muscle.
  • Insufficient blood supply to the myocardium can result in myocardial ischemia, injury or infarction, or all three. Atherosclerosis of the larger coronary arteries is the most common anatomic condition to diminish coronary blood flow. The branches of coronary arteries arising from the aortic root are distributed on the epicardial surface of the heart. These in turn provide intramural branches that supply the cardiac muscle. Myocardial ischemia generally appears first and is more extensive in the sub-endocardial region since these deeper myocardial layers are farthest from the blood supply, with greater intramural tension and need for oxygen.
  • The term infarction describes necrosis or death of myocardial cells. Atherosclerotic heart disease is the most common underlying cause of myocardial infarction. The left ventricle is the predominant site for infarction; however, right ventricular infarction occasionally coexists with infarction of the inferior wall of the left ventricle. The appearance of pathological Q waves is the most characteristic ECG finding of transmural myocardial infarction of the left ventricle. A pathological Q wave is defined as an initial downward deflection of a duration of 40 msec or more in any lead except III and aVR. The Q wave appears when the infarcted muscle is electrically inert and the loss of forces normally generated by the infarcted area leaves unbalanced forces of variable magnitude in the opposite direction from the remote region, for example, an opposite wall. These forces can be represented by a vector directed away from the site of infarction and seen as a negative wave (Q wave) by electrodes overlying the infarcted region.During acute myocardial infarction, the central area of necrosis is generally surrounded by an area of injury, which in turn is surrounded by an area of ischemia. Thus, various stages of myocardial damage can coexist. The distinction between ischemia and necrosis is whether the phenomenon is reversible. Transient myocardial ischemia that produces T wave, and sometimes ST segment abnormalities, can be reversible without producing permanent damage and is not accompanied by serum enzyme elevation. Two types of myocardial infarction can be observed electrocardiographically:Q wave infarction, which is diagnosed by the presence of pathological Q waves and is also called transmural infarction. However, transmural infarction is not always present; hence, the term Q-wave infarction may be preferable for ECG description , Non-Q wave infarction, which is diagnosed in the presence of ST depression and T wave abnormalities.
  • The term infarction describes necrosis or death of myocardial cells. Atherosclerotic heart disease is the most common underlying cause of myocardial infarction. The left ventricle is the predominant site for infarction; however, right ventricular infarction occasionally coexists with infarction of the inferior wall of the left ventricle. The appearance of pathological Q waves is the most characteristic ECG finding of transmural myocardial infarction of the left ventricle. A pathological Q wave is defined as an initial downward deflection of a duration of 40 msec or more in any lead except III and aVR. The Q wave appears when the infarcted muscle is electrically inert and the loss of forces normally generated by the infarcted area leaves unbalanced forces of variable magnitude in the opposite direction from the remote region, for example, an opposite wall. These forces can be represented by a vector directed away from the site of infarction and seen as a negative wave (Q wave) by electrodes overlying the infarcted region.During acute myocardial infarction, the central area of necrosis is generally surrounded by an area of injury, which in turn is surrounded by an area of ischemia. Thus, various stages of myocardial damage can coexist. The distinction between ischemia and necrosis is whether the phenomenon is reversible. Transient myocardial ischemia that produces T wave, and sometimes ST segment abnormalities, can be reversible without producing permanent damage and is not accompanied by serum enzyme elevation. Two types of myocardial infarction can be observed electrocardiographically:Q wave infarction, which is diagnosed by the presence of pathological Q waves and is also called transmural infarction. However, transmural infarction is not always present; hence, the term Q-wave infarction may be preferable for ECG description , Non-Q wave infarction, which is diagnosed in the presence of ST depression and T wave abnormalities.
  • The absence of reciprocal changes does not mean the patient is not experiencing an MI. The presence of reciprocal changes, however, is highly indicative of an acute myocardial infarction.
  • The absence of reciprocal changes does not mean the patient is not experiencing an MI. The presence of reciprocal changes, however, is highly indicative of an acute myocardial infarction.
  • Because of the location of the coronary arteries, Septal Mis almost always have anterior extension.
  • Nitro resolves ST-Elevation
  • Here are two 12-leads performed on the same patient 15 minutes apart. ECG A was performed before ECG B. Can you see the suttle differences? Is this a dynamic MI?
  • Here are two 12-leads performed on the same patient 15 minutes apart. ECG A was performed before ECG B. Can you see the subtle differences? Is this a dynamic MI?
  • Anterioseptal MI
  • Arm lead reversal, axis about 180
  • Arm lead reversal, axis about 180
  • A PVC Every 3 beats is considered trigeminal
  • A PVC Every 3 beats is considered trigeminal
  • A PVC Every 3 beats is considered trigeminal
  • Shaded out all premature beats
  • 12 lead-lesson 5

    1. 1. 12-LeadElectrocardiography a comprehensive course sson5 Le Adam Thompson, EMT-P, A.S.
    2. 2. The 6-Step Method• 1. Rate & Rhythm• 2. Axis Determination• 3. Intervals• 4. Morphology• 5. STE-Mimics• 6. Ischemia, Injury, & Infarct
    3. 3. Lesson Five• STEMI – ST-Segment Elevated Myocardial Infarction – ST-Segment Elevation of > 1mm in two contiguous leads. – In V2 & V3, ST-Segment elevation must be at least 2mm. *The smaller the QRS complex, the more significant minimal ST- Elevation is.
    4. 4. Objectives• Learn how to identify a STEMI• Learn how to localize the infarcted area• Apply everything learned thus far
    5. 5. What are Contiguous Leads?Lead I aVR V1 V4 • lateral Contiguous leads are leads that look at septal anterior the same area of the heart.Lead II aVL V2 V5 •inferior show up on the 12-lead proximal They high lateral septal low lateral to each other.Lead III aVF V3 V6 inferior inferior anterior low lateral
    6. 6. Coronary CirculationRight Coronary Artery Left Main (RCA) Circumflex (LCx)Left Anterior Descending (LAD)
    7. 7. Coronary Circulation Right Coronary Artery Left Circumflex Artery Left Anterior Descending (RCA) (LCx) (LAD)•Right Atrium •Inferior Wall •Anterior•Inferior Wall •Isolated Right Ventricle •Anteroseptal•Inferior-Right Ventricle •Posterior Wall •Anteroseptal-lateral•Posterior Wall - 15% of population - 85% of population •Anterolateral •Inferolateral •Posterolateral *Nicknamed “Widow-maker”
    8. 8. Coronary Occlusion
    9. 9. Heart Anatomy SeptalAnterior Lateral WallInferior
    10. 10. Heart AnatomyEndocardium Epicardium Myocardium
    11. 11. Ischemia, Injury, Infarct
    12. 12. ST-Elevation• The most common cause of ST- elevation is not myocardial infarction.• Less than 50% of STEMI alerts called by paramedics are actually Acute Coronary Syndrome (ACS) patients
    13. 13. ST-Elevation TP-Segment• ST-Elevation is elevation of the J-Point which causes elevation of the following ST- Segment.• Elevation is defined as anything above the T P isoelectric line.• Find the isoelectric line by locating the TP- Segment.
    14. 14. ST-Elevation• The J-Point is where the QRS complex J-Point and the ST-Segment meet.
    15. 15. ST-Segment Morphology Concave Convex J-Point J-Point
    16. 16. Evolution of MI• Insufficient blood supply to the myocardium. – Ischemia, injury or infarction, or all three.• The branches of coronary arteries arising from the aortic root are distributed on the epicardial surface of the heart.• These in turn provide intramural branches that supply the cardiac muscle.• Myocardial ischemia generally appears first.
    17. 17. Evolution of MIIschemi Injury InfarctionaNeeds O2 Damage from Irreversible lack of O2 damage
    18. 18. Ischemia• Subendocardial ischemia – Ischemia in this area prolongs local recovery time. Since repolarization normally proceeds in an epicardial-to-endocardial direction, delayed recovery in the subendocardial region due to ischemia does not reverse the direction of repolarization but merely lengthens it.
    19. 19. Ischemia• Transmural ischemia – is said to exist when ischemia extends subepicardially. This process has a more visible effect on recovery of subepicardial cells compared with subendocardial cells. Recovery is more delayed in the subepicardial layers, and the subendocardial muscle fibers seem to recover first.
    20. 20. Ischemia• Hyperacute T-Waves – Results from subendocardial ischemia – Symmetrical & tall – Wide with blunt peak (unlike Hyperkalemia) – Present for about first 30 min. of AMI• Inverted T-waves – Results from transmural ischemia
    21. 21. IschemiaAsymmetricalSymmetrical
    22. 22. Ischemia
    23. 23. Ischemia-Mimic Hyperkalemia STE-Mimic Inverted T-WavesPeaked T-Waves
    24. 24. Injury• Injury to the myocardial cells results when the ischemic process is more severe.• In patients with coronary artery disease, ischemia, injury and myocardial infarction of different areas frequently coexist, producing mixed and complex ECG patterns.
    25. 25. Injury• ST-Depression – Subendocardial• ST-Elevation – Subepicardial – Transmural.
    26. 26. Injury
    27. 27. Injury ST-ElevationST-Depression
    28. 28. Injury-MimicHyperkalemia STE-Mimic ST-Elevation
    29. 29. Infarct• The term infarction describes necrosis or death of myocardial cells.• Atherosclerotic heart disease is the most common underlying cause of myocardial infarction.• The left ventricle is the predominant site for infarction; however, right ventricular infarction occasionally coexists with infarction of the inferior wall of the left ventricle.
    30. 30. Infarct• During acute myocardial infarction, the central area of necrosis is generally surrounded by an area of injury, which in turn is surrounded by an area of ischemia.• Various stages of myocardial damage can coexist.• The distinction between ischemia and necrosis is whether the phenomenon is reversible.
    31. 31. Infarct• Pathological Q-waves – Wider than 0.04sec / 40ms (1 small box) – Deeper than 25% the height of R-Wave
    32. 32. Reciprocal Changes Site Facing Reciprocal• ST-Depression found in leads opposite Septal V1, V2 V7, V8, V9 ofAnterior with ST-Elevation is considered those V3, V4 None toLateral reciprocal change. be a I, aVL, V5, V6 II, III, aVF – This is caused by III, view from the opposite a aVF Inferior II, I, aVL direction. Posterior V7, V8, V9 V1, V2
    33. 33. Reciprocal ChangesReciprocal ST-Depression QuickTime™ and a decompressor are needed to see this picture. Inferior Injury
    34. 34. Location of MI Septal Anterior Wall Lateral WallInferior Wall
    35. 35. Location of MI Left VentricleRight Ventricle
    36. 36. Antero-Septal Wall• Leads V1 & V2 view the septal wall• Leads V3 & V4 view the anterior wall LV V6 RV V5 V4 V1 V3 V2
    37. 37. Septal Wall
    38. 38. Anterior Wall• Leads V3 & V4 view the Anterior Wall LV V6 RV V5 V4 V1 V3 V2
    39. 39. Anterior Wall
    40. 40. Lateral Wall• Leads I, aVL, V5 & V6 view the lateral wall LV V6 RV V5 V4 V1 V3 V2
    41. 41. Lateral Wall
    42. 42. Inferior WallInferior Wall
    43. 43. Inferior Wall
    44. 44. Inferior Wall
    45. 45. Right Ventricular Wall• With a proximal occlusion of the RCA, a right ventricular infarct is possible. – Hypotension is most common finding. – Right-sided placement of V3 & V4 can be used to view the right ventricle for ST-Elevation. • V4R is most sensitive lead for right-sided changes. • QRS complexes and ST-Elevation may be of much lesser amplitude in right-sided leads.
    46. 46. Right Ventricular Wall• Hypotension is most common assessment finding with RV-Infarction. – NTG should be used very conservatively – Fluids should be administered if unstable• ST-Elevation in lead III > than STE in lead II is very specific for RV-Infarction
    47. 47. Right Ventricular Wall Move V3 & V4 to mirrored position on right side of chest to obtain V3R & V3 V4R.V4 The same can be done for V5 & V6.
    48. 48. Right Ventricular Wall I aVR V1 V4RAlways make II aVL V2 V7sure to denotethe leads you III aVF V3R V6change.
    49. 49. Posterior Wall• Dominant RCA – When the RCA supplies the posterior descending coronary artery – 85% of people have dominant RCA• Dominant Circumflex – When LCx supplies the posterior descending coronary artery – 15% of people have dominant circumflex
    50. 50. Posterior Wall• The reciprocal leads are V1 & V2• ST-depression in V1 & V2 may actually be representing ST-elevation of the posterior wall• Tall R-waves in V1 & V2 may actually be representing pathological Q-waves of the posterior wall
    51. 51. Posterior WallV1/V2 To identify a posterior wall MI, a technique commonly taught is to pretend you are looking at the complex upside-down through a mirror
    52. 52. Posterior Wall V7, V8, V9 I aVR V1 V7 II aVL V2 V8 III aVF V3 V9Move V4 to V7 - posterior axillary lineMove V5 to V8 - midscapularMove V6 to V9 paraspinal
    53. 53. LBBB With MIModified Sgarbossa’s criteria• Any concordant ST-Elevation!• ST-Elevation > 25% of depth of preceding S- Wave = MI – This is an advanced skill, and is completely reliant on the T-wave discordance found with a LBBB• This same criteria may be used with paced rhythms
    54. 54. Sgarbossa’s Criteria
    55. 55. Sgarbossa’s Criteria
    56. 56. Other MI Findings• If ECG print out does not read ***Acute MI***, it is highly unlikely that the capture meets STEMI criteria. – It is possible that the 12-lead is not a true STEMI even with the “Acute AMI” reading.• Wellen’s phenomenon - Biphasic or inverted T-waves (Most commonly in V2 & V3), precursor to AMI from LAD stenosis.
    57. 57. Practice
    58. 58. RBBB With MI
    59. 59. Practice
    60. 60. Antero-septal MI
    61. 61. Antero-septal MIAB
    62. 62. Practice
    63. 63. Anterior MI
    64. 64. PracticeAB
    65. 65. Inferior MI
    66. 66. Practice
    67. 67. Inferior MI
    68. 68. Practice
    69. 69. Antero-septal MI
    70. 70. Practice
    71. 71. RBBB, Inferior MI
    72. 72. Practice
    73. 73. Practice
    74. 74. RBBBNo ST-Elevation!
    75. 75. Practice29 y/o Male
    76. 76. WPW29 y/o Male
    77. 77. PracticeAB
    78. 78. Practice
    79. 79. PracticeA RB R
    80. 80. PracticeA RB R
    81. 81. Inferior-Posterior MIA RB R
    82. 82. Practice
    83. 83. Antero-septal MIAB
    84. 84. Practice
    85. 85. Bigeminy Anterior MI
    86. 86. Practice
    87. 87. Antero-septal-lateral MI
    88. 88. Practice Scenarios“Always consider the company it keeps” - Dr. Thomas Garcia
    89. 89. Practice Scenario 1• You respond to an 87 year-old female who states that she awoke with “a fast heart rate”.• She states that she has had this condition for over 50 years, and denies any pain or dyspnea.• She has had heart surgery in the past.
    90. 90. Practice Scenario 1• No abnormal physical exam findings• BP: 156/74• HR: 124 irregularly irregular• O2 Sat:96% on room air
    91. 91. Practice Scenario 1
    92. 92. Practice Scenario 2• You respond to a 51 year-old female who reportedly became unconscious and slumped over in a chair.• Family states that she has been unconscious for 5 minutes.• She has a history of hypertension and takes Xanax and hydrochlorothiazide.
    93. 93. Practice Scenario 2• She is flushed and diaphoretic• She is awake but disoriented• BP: 180/120• HR: 110 Regular• Respirations: 16• O2 Sat: 95%
    94. 94. Practice Scenario 2
    95. 95. Practice Scenario 3• You respond to a 94 year-old female in a nursing home.• She had a syncopal episode per the LPN, and is currently complaining of unlocalized pain.
    96. 96. Practice Scenario 3• She is pale but dry• BP: 142/57• HR: 88• Respirations: 24• O2 Sat: 88% on High-flow O2
    97. 97. Practice Scenario 3
    98. 98. Practice Scenario 3
    99. 99. Practice
    100. 100. Trigeminal PVCsPossible Antero-septal Infarct
    101. 101. Trigeminal PVCs
    102. 102. Trigeminal PVCs
    103. 103. Lesson 5• This concludes lesson 5• Please review the course materials

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