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• 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.
• In this lesson, we are going to perform the third and fourth steps of the six step method.
• Lets try to get a pretty acurate Axis
• Does this image look familiar. We start by finding our equiphasic lead.
• Lead III has some ST depression, but looks to be the most equiphasic lead.
• We find lead III on our hexaxial reference system. Now we need to figure out which lead is perpindicular to lead III
• Remember. When the heart ’s mean electrical vector (or QRS axis) moves toward a positive electrode, you get an upright complex in that lead. When it moves away from a positive electrode, you get a negative complex in that lead. When it moves perpendicular to a positive electrode, you get an equiphasic (and/or isoelectric) complex in that lead.
• Since lead III is equiphasic, that means it is perpendicular to the heart’s mean electrical exis in the frontal plane. So we find the lead that is perpendicular to lead III because it will be the most in line with the heart’s mean electrical axis. aVR is perpendicular to lead III. So the axis is close to either -150 or 30 degrees. To figure out which one, we need to see if lead aVR is positive or negative.
• We see that aVR is negative, so we look at the down arrow on the reference system.
• The down arrow is at the 30 degree mark, so our frontal axis is about 30 degrees.
• 30 degrees falls in the normal frontal Axis range!
• The monitor found an R-axis at 34 degrees, so our conclusion of 30 degrees is pretty damn close. What about our precordial axis?
• Since with normal physiology, the transition zone is in the area of V3 or V4, lets put an arrow in that direction.
• It looks like the QRS goes from being all negative to all positive between V3 &amp; V4. This is normal.
• Ok, we are on to the third and fourth steps of the 6 step method. We assess our intervals and morphology.
• Our intervals look to be within a normal range, the QRS is less than 120ms, the PR-interval is less than 200 ms, and the QTc is less than 460 ms. There does appear to be a biphasic P-wave in V1, but this is probably just indicative of LAE. The most obvious abnormality is those Symmetrical, broad and tall T-Waves in V2 &amp; V3, do you remember a pathology that can cause these?
• Remember, hyperkalemic T-waves are usually narrow with a sharp peak. These look very much like hyperacute T-waves; which we know are an early sign of a heart attack. We can’t call this a STEMI based on their presence, but they certainly heighten our degree of suspicion. Lets move on to our next step.
• We do note some ST-elevation, although it isn’t in contiguous leads. The ST-elevation is present minimally in aVL, and significantly in V1. We can determine how much in V1 by finding our J-point in a lead below it and drawing a line.
• We also mark our isoelectric line in V1 by conecting the TP-segments to determine how elevated the ST-segment is in V1. We see that the elevation is at least 2mm in V1. Is their a STE-Mimic present?
• We already said that the T-wave amplitude is not due to hyperkalemia. The ST-elevation is only in two leads and it is convex, so it probably isn’t related to pericarditis or early repol. We do have T-wave discordance in all of the precordial leads, but the QRS is too narrow for a LBBB and the amplitude isn’t great enough for LVH, so it probably isn’t LV-strain. This ECG doesn’t appear to have a STE-Mimic. Lets move on to the final step to determine if this ECG has evidence of ischemia, injury, or infarct.
• Our ST-elevation is not in contiguous leads
• We note ST-Elevation, but since it isn’t in two contiguous leads, it doesn’t meet STEMI criteria. We have also discovered Hyperacute T-waves, and it looks like there is some ST-depression in the inferior leads. This could be a reciprocal change or a sign of subendocardial injury. This ECG may not meet STEMI criteria, but we can certainly start our ACS treatment and begin transporting this patient to a cardiac facility based on these findings; especially in the presence of chest pain. We should also make sure to do repeat 12-leads on the way in!
• Our ST-depression is in the inferior leads, II, III, and aVF, so it would make sense to see some elevation in I, aVL, V5, or V6
• Here is the next 12-Lead we capture. Do you see the obvious difference??? Lets look at them both together to see how significant the changes are.
• We now have an obvious Antero-Septal MI that meets STEMI criteria. Whenever you have ECG changes like this, you can be certain you are dealing with a significant cardiac event. Look at the exponential increase in ST-elevation from the first ECG to the second. The precordial axis even shifted slightly between both leads. Look at how V4 changes in amplitude. This type of convex ST-elevation is always significant! And this case proves how important it is to aquire more than one single 12-lead.
• Take a look at the graphic here. If the terminal wave of the QRS is positive in V1 it is a RBBB. If the terminal wave of the QRS is negative in V1 it is a LBBB. This is assuming that it is a wide atrial rhythm.
• Here is a chart to make things easier.
• The monitor looks to have an accurate reading for the rate on this relatively clean ECG tracing. The HR looks to be right around 70. Our PR interval is just slightly longer than 200ms, or one big box, which brings us into that 1st degree AV block range. We now have our rate &amp; rhythm. Lets use the quadrant method to determine our axis in the frontal plane.
• The monitor looks to have an accurate reading for the rate on this relatively clean ECG tracing. The HR looks to be right around 70. Our PR interval is just slightly longer than 200ms, or one big box, which brings us into that 1st degree AV block range. We now have our rate &amp; rhythm. Lets use the quadrant method to determine our axis in the frontal plane.
• The monitor looks to have an accurate reading for the rate on this relatively clean ECG tracing. The HR looks to be right around 70. Our PR interval is just slightly longer than 200ms, or one big box, which brings us into that 1st degree AV block range. We now have our rate &amp; rhythm. Lets use the quadrant method to determine our axis in the frontal plane.
• The monitor looks to have an accurate reading for the rate on this relatively clean ECG tracing. The HR looks to be right around 70. Our PR interval is just slightly longer than 200ms, or one big box, which brings us into that 1st degree AV block range. We now have our rate &amp; rhythm. Lets use the quadrant method to determine our axis in the frontal plane.
• The monitor looks to have an accurate reading for the rate on this relatively clean ECG tracing. The HR looks to be right around 70. Our PR interval is just slightly longer than 200ms, or one big box, which brings us into that 1st degree AV block range. We now have our rate &amp; rhythm. Lets use the quadrant method to determine our axis in the frontal plane.
• The monitor looks to have an accurate reading for the rate on this relatively clean ECG tracing. The HR looks to be right around 70. Our PR interval is just slightly longer than 200ms, or one big box, which brings us into that 1st degree AV block range. We now have our rate &amp; rhythm. Lets use the quadrant method to determine our axis in the frontal plane.
• The monitor looks to have an accurate reading for the rate on this relatively clean ECG tracing. The HR looks to be right around 70. Our PR interval is just slightly longer than 200ms, or one big box, which brings us into that 1st degree AV block range. We now have our rate &amp; rhythm. Lets use the quadrant method to determine our axis in the frontal plane.
• The monitor looks to have an accurate reading for the rate on this relatively clean ECG tracing. The HR looks to be right around 70. Our PR interval is just slightly longer than 200ms, or one big box, which brings us into that 1st degree AV block range. We now have our rate &amp; rhythm. Lets use the quadrant method to determine our axis in the frontal plane.
• Now look at the R-wave progression within the precordial leads. Notice the early R-wave progression, or counterclockwise rotation of the precordial axis?
• Now look at the R-wave progression within the precordial leads. Notice the early R-wave progression, or counterclockwise rotation of the precordial axis?
• Now look at the R-wave progression within the precordial leads. Notice the early R-wave progression, or counterclockwise rotation of the precordial axis?
• Now look at the R-wave progression within the precordial leads. Notice the early R-wave progression, or counterclockwise rotation of the precordial axis?
• We already identified a prolonged PR-Interval. Do you notice any other prolonged intervals? What about the QRS complex? Is it wider than 120 ms? The monitor seems to think so, it estimated the QRS duration at about 156 ms That is wide! Luckily, we know we have P-waves, indicating that the SA node is controlling the rhythm. What causes a wide QRS complex with a supraventricular rhythm?
• Did you say bundle branch block? That’s right. So what kind are we dealing with?? Lets look at the terminal waves in V1, lead I, and V6.
• We have a terminal R-wave in V1 which indicates a RBBB, the small terminal S-wave in V6 and the bigger one in lead 1 both provide conclusive evidence that this is, in fact, a RBBB. Remember that list of pathologies assosciated with axis deviation?
• RBBB happens to be a cause of both types of axis deviation we have already identified. See how this stuff comes together??
• Now we determine if any STE-Mimics exist. Well, we know a RBBB can be a STE-Mimic, lets see if we see any ST-Elevation.
• Now we determine if any STE-Mimics exist. Well, we know a RBBB can be a STE-Mimic, lets see if we see any ST-Elevation.
• Now we determine if any STE-Mimics exist. Well, we know a RBBB can be a STE-Mimic, lets see if we see any ST-Elevation.
• Now we look for any indication of ischemia, injury, or infarct.
• The only leads that don’t follow the appropriate rule of T-wave discordance are V2 &amp; V3. It looks like the ST-elevation has taken the T-wave with it. That is exactly what happens when you have a myocardial insult with a BBB. V2 &amp; V3 require at least 2mm of ST-elevation to meet STEMI criteria, but that is because these are usually the most discordant leads with a normal precordial axis. In this situation, this amount of ST-elevation is significant and the patient should be appropriately treated for an MI. Lets look at the second ECG.
• Our second ECG confirms our suspicions of a coronary insult. We can now see some obvious ST-Elevation, and hyperacute T-waves.
• Our second ECG confirms our suspicions of a coronary insult. We can now see some obvious ST-Elevation, and hyperacute T-waves.
• Looks like the transition happens around V3, which is normal.
• The only abnormal interval is the slightly shortened PR-interval which makes us consider accessory pathways, or a possible junctional rhythm. Nothing clinically significant at this point, but worth considering if the rate becomes more rapid and needs to be managed. The symmetrical T-waves also indicate a pathology. At this point we don’t know which one, but they are worth noting.
• Don’t see any ST-elevation, so we aren’t really concerned to much about a STE-Mimic right now. Lets review our list of STE-Mimics though.
• Don’t see any ST-elevation, so we aren’t really concerned to much about a STE-Mimic right now. Lets review our list of STE-Mimics though.
• We have already noted the symmetrical T-waves. Also worth noting are the inverted T-waves in aVL, &amp; V1. Those leads often have meaningless inverted T-waves though. We obviously don’t have a STEMI here. We are concerned about the hypotension, and these slight changes that we have discovered definitely indicate the need for serial 12-leads.

1. 1. 12-LeadElectrocardiography a comprehensive course sson6 Le Adam Thompson, EMT-P, A.S.
2. 2. Lesson Six• Review Wide Complex Tachycardia (WCT)• Briefly discuss treatment strategies for arrhythmias• Discuss paced rhythms• Practice the 6-Step method of ECG interpretation
3. 3. Objectives• Learn how to apply an appropriate treatment strategy for wide complex tachycardias.• Learn how to identify paced rhythms• Apply all skills learned throughout the course.
4. 4. The 6-Step Method• 1. Rate & Rhythm• 2. Axis Determination• 3. Intervals• 4. Morphology• 5. STE-Mimics• 6. Ischemia, Injury, & Infarct
5. 5. Wide Complex Tachycardia• Ventricular Tachycardia• SVT with aberrancy – Bundle Branch Block – Accessory Pathway (WPW/LGL)
6. 6. Wide Complex TachycardiaAll WCTs are Ventricular Tachycardia until PROVEN otherwise!
7. 7. Treatment Strategy• If unstable, SHOCK!• If stable – Try to determine if supraventricular or not. – Unsure? Treat as Ventricular Tachycardia!
8. 8. Treatment Strategy
9. 9. Wide Complex Tachycardia• There are many indicators that rule VT in, but very few that rule VT out.
10. 10. Wide Complex Tachycardia • Factors that favor V-Tach – AV Dissociation – Capture Beats & Fusion Beats – Non-conducted P-waves – A regular rhythm – QRS Morphology • wide, Brugada’s, Josephson’s – Extreme Right Axis Deviation – Concordance in precordial leads – History of MI, CHF, or structural heart disease – Physical Exam • Cannon A-Waves, no vagal response
11. 11. AV Dissociation• Different than 3rd degree AVB – Ventricular depolarization is faster than atrial depolarization (more QRS complexes than P-waves)• No correlation between P-wave & QRS complex
12. 12. Capture Beats• In the presence of AV dissociation.• When the atrial depolarization triggers a single QRS complex of different morphology than the rest• The complex is narrow with a preceding P-wave.
13. 13. Fusion Complexes• In the presence of AV dissociation.• When the atrial depolarization and ventricular depolarization both occur at the same time, fusing together both of their complexes.• Will look different than the rest of the QRS- complexes
14. 14. Non-Conducted P-Waves• Atrial-ventricular dissociation• Upright P-waves in leads II, III, or aVF tell us that the atrial depolarization is coming from right atrium.
15. 15. Regularity• Monomorphic ventricular tachycardia is very regular.• Polymorphic ventricular tachycardia appears bizarre and irregular• Torsades de Pointes has an unmistakable pattern
16. 16. QRS Width• A QRS width of greater than 140 ms tips the scale heavily in favor of V-tach.• Brugada’s Sign – Interval from beginning of QRS to tip of S- wave (Nadir) > 100 ms (0.10 sec)
17. 17. Josephson’s Sign• A notch or slurring on the down-slope of the S-wave
18. 18. Josephson’s SignJosephson’s Sign
19. 19. QRS Morphology• In Lead V1 – R > R’ – If the first R-wave is taller than the second R-wave in V1, V-tach is highly likely. – This is just one possible morphology of VT.
20. 20. QRS MorphologyRBBB Morphology VT Morphology V1 V1
21. 21. QRS Morphology• PVCs of similar morphology favors VT – The presence of a supraventricular rhythm with PVCs that changes to a WCT, and the QRS morphology looks similar to the previous PVCs.
22. 22. ERAD• Extreme Right Axis Deviation – A frontal axis of -90° to -180° – Negative QRS in lead I & aVF
23. 23. ERAD Extreme Right AxisI aVR V1 V4II aVL V2 V5II aVF V3 V6
24. 24. Precordial Concordance• QRS Concordance in Precordial Leads – Every QRS complex is positive, or – Every QRS complex is negative
25. 25. Precordial Concordance Positive ConcordanceI aVR V1 V4II aVL V2 V5II aVF V3 V6
26. 26. Precordial Concordance Negative ConcordanceI aVR V1 V4II aVL V2 V5II aVF V3 V6
27. 27. Past Medical History• Significant cardiac history is suggestive of ventricular tachycardia – Long list of cardiac meds – Previous heart attack – Previous episodes of v-tach
28. 28. Physical Exam• Cannon A-Waves – Observable pulsations in the neck that indicate complete AV dissociation.• Vagal Response – The vagus nerve does not innervate the ventricles. – Vagal maneuvers will only work in the presence of a supraventricular rhythm.
29. 29. SVT With RBBB
30. 30. Ventricular Tachycardia
31. 31. WCT Change
32. 32. Practice• Lets take a look at some 12-Lead recordings and use the 6-step method to interpret them.
33. 33. 62 y/o MaleComplaining of Chest Pain
34. 34. 62 y/o MaleRate & Rhythm
35. 35. Rate: 88 Normal Sinus62 y/o Male Axis
36. 36. 62 y/o Male
37. 37. Rate: 88 Normal Sinus62 y/o Male Axis
38. 38. 62 y/o Male
39. 39. Hexaxial Reference System + + A B A + B• When the mean axis is perpendicular to the positive electrode, the QRS is equiphasic.
40. 40. 62 y/o Male
41. 41. Rate: 88 Normal Sinus62 y/o Male Axis
42. 42. 62 y/o Male
44. 44. Rate: 88 Normal Sinus Frontal Axis: 30°62 y/o Male Axis
45. 45. Precordial Axis V1 V2 V3 V4 V5 V6Normal transition
46. 46. Rate: 88 Normal Sinus Frontal Axis: 30°62 y/o Male Axis
47. 47. Rate: 88 Normal Sinus Frontal Axis: 30° Precordial Axis: Normal 62 y/o MaleIntervals & Morphology
48. 48. Rate: 88 Normal Sinus Frontal Axis: 30° Precordial Axis: Normal 62 y/o MaleIntervals & Morphology
49. 49. Rate: 88 Normal Sinus Frontal Axis: 30° Precordial Axis: Normal 62 y/o MaleIntervals & Morphology Hyperacute T-Waves
50. 50. Rate: 88 Normal Sinus Frontal Axis: 30° Precordial Axis: Normal Hyperacute T-waves62 y/o Male STE-Mimics
51. 51. Rate: 88 Normal Sinus Frontal Axis: 30° Precordial Axis: Normal Hyperacute T-waves62 y/o Male STE-Mimics
52. 52. Rate: 88 Normal Sinus Frontal Axis: 30° Precordial Axis: Normal Hyperacute T-waves62 y/o Male STE-Mimics
53. 53. Rate: 88 Normal Sinus Frontal Axis: 30° Precordial Axis: Normal Hyperacute T-waves 62 y/o Male STE-MimicsLead I aVR V1 V4 lateral septal anteriorLead II aVL V2 V5 inferior high lateral septal low lateralLead III aVF V3 V6 inferior inferior anterior low lateral
54. 54. Rate: 88 Normal Sinus Frontal Axis: 30° Precordial Axis: Normal Hyperacute T-waves 62 y/o MaleIschemia, Injury, Infarct
55. 55. Rate: 88 Normal Sinus Frontal Axis: 30° Precordial Axis: Normal Hyperacute T-waves 62 y/o Male Ischemia, Injury, InfarctSite Facing
56. 56. Rate: 88 Normal Sinus Frontal Axis: 30° Precordial Axis: Normal Hyperacute T-waves62 y/o Male 12-Lead #2
57. 57. Rate: 88 Normal Sinus Frontal Axis: 30° Precordial Axis: Normal Hyperacute T-waves62 y/o Male Antero-Septal MI
58. 58. 72 y/o Female Recent Syncope QuickTime™ and a decompressor are needed to see this picture.
59. 59. 72 y/o Female Rate & Rhythm
60. 60. 72 y/o Female Rate & Rhythm 10 Seconds
61. 61. 72 y/o Female Rate & Rhythm1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 10 Seconds
62. 62. 72 y/o Female Rate & Rhythm1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 19 x 6 = 114 10 Seconds
63. 63. Rate: 11472 y/o Female Rate & Rhythm
64. 64. Rate: 114 Sinus Tachycardia72 y/o Female Rate & Rhythm
65. 65. Rate: 114 Sinus Tachycardia72 y/o Female Axis
66. 66. Cheat Sheet Normal Physiologic Pathologic Right Axis Extreme Indeterminate Axis Left Left Right Axis Axis 0° to 90° 0° to -30° -30° to -90° 90° to 180° -90° to 180° ?Lead ILead IILead III
67. 67. Rate: 114 Sinus Tachycardia Frontal Axis: Normal72 y/o Female Axis
68. 68. Rate: 114 Sinus Tachycardia Frontal Axis: Norma Clockwise Rotation 72 y/o FemaleIntervals & Morphology
69. 69. Bundle Branch BlocksV1 = RBBBV1 = LBBB
70. 70. BBB Chart RBBB LBBB IVCD V1 TERMINAL TERMINAL TERMINAL R-WAVE S-WAVE R/S-WAVEI & V6 TERMINAL TERMINAL Anything is possible S-WAVE R-WAVE
71. 71. Rate: 114 Sinus Tachycardia Frontal Axis: Norma Clockwise Rotation 72 y/o Female LBBBIntervals & Morphology
72. 72. Rate: 114 Sinus Tachycardia Frontal Axis: Norma Clockwise Rotation72 y/o Female LBBB STE-Mimics
73. 73. Rate: 114 Sinus Tachycardia Frontal Axis: Norma Clockwise Rotation 72 y/o Female LBBBIschemia, Injury, Infarct
74. 74. 73 y/o Male Diaphoresis
75. 75. 73 y/o MaleRate & Rhythm
76. 76. Rate: 71 Normal Sinus - 1st° AVB73 y/o Male Axis
77. 77. Rate: 71 Normal Sinus - 1st° AVB 73 y/o Male Axis -90° ERAD LAD180° 0° RAD Normal 90°
78. 78. Rate: 71 Normal Sinus - 1st° AVB73 y/o Male Axis
79. 79. Rate: 71 Normal Sinus - 1st° AVB 73 y/o Male Axis aVF --I I+ aVF +
80. 80. Rate: 71 Normal Sinus - 1st° AVB73 y/o Male Axis
81. 81. Rate: 71 Normal Sinus - 1st° AVB 73 y/o Male Axis aVF --I I+ aVF +
82. 82. Rate: 71 Normal Sinus - 1st° AVB 73 y/o Male Axis aVF --I I+ aVF +
83. 83. Rate: 71 Normal Sinus - 1st° AVB 73 y/o Male Axis -90° ERAD LAD180° 0° RAD Normal 90°
84. 84. Rate: 71 Normal Sinus - 1st° AVB Right Axis Deviation73 y/o Male Axis
85. 85. Rate: 71 Normal Sinus - 1st° AVB Right Axis Deviation Early R-Wave Progression73 y/o Male Axis
86. 86. Rate: 71 Normal Sinus - 1st° AVB Right Axis Deviation Early R-Wave Progression 73 y/o Male Frontal Plane Axis Axis Precordial Axis ERAD Right Axis Pathological Early Transition Late Transition Deviation Left Axis Counterclockwise Clockwise -90° to 180° Deviation Rotation Rotation 90° to 180° -30° to -90°• Ventricular • May be normal • Pregnancy • Posterior wall • SometimesRhythm • LPFB • LAFB infarction Normal,• Paced Rhythm • RVH especially in • Pulmonary • WPW• Dextrocardia • RBBB women disease • Pulmonary • Anterior MI• Electrolyte • RVH diseasederangement • LVH • RBBB • LBBB • LAFB • WPW • Hyperkalemia • LBBB • Dextrocardia • Q-waves, MI • Lung Disease •Venrticular Rhythm
87. 87. Rate: 71 Normal Sinus - 1st° AVB Right Axis Deviation Early R-Wave Progression 73 y/o MaleIntervals & Morphology
88. 88. Rate: 71 Normal Sinus - 1st° AVB Right Axis Deviation Early R-Wave Progression 73 y/o MaleIntervals & Morphology
89. 89. Rate: 71 Normal Sinus - 1st° AVB Right Axis Deviation Early R-Wave Progression 73 y/o MaleIntervals & Morphology
90. 90. Rate: 71 Normal Sinus - 1st° AVB Right Axis Deviation Early R-Wave Progression 73 y/o MaleIntervals & Morphology
91. 91. Rate: 71 Normal Sinus - 1st° AVB Right Axis Deviation Early R-Wave Progression 73 y/o Male Intervals & Morphology Frontal Plane Axis Precordial Axis ERAD Right Axis Pathological Early Transition Late Transition Deviation Left Axis Counterclockwise Clockwise -90° to 180° Deviation Rotation Rotation 90° to 180° -30° to -90°• Ventricular • May be normal • Pregnancy • Posterior wall • SometimesRhythm • LPFB • LAFB infarction Normal,• Paced Rhythm • RVH especially in • Pulmonary • WPW• Dextrocardia • RBBB women disease • Pulmonary • Anterior MI• Electrolyte • RVH diseasederangement • LVH • RBBB • LBBB • LAFB • WPW • Hyperkalemia • LBBB • Dextrocardia • Q-waves, MI • Lung Disease •Venrticular Rhythm
92. 92. Rate: 71 Normal Sinus - 1st° AVB Right Axis Deviation Early R-Wave Progression73 y/o Male RBBB STE-Mimics
93. 93. Rate: 71 Normal Sinus - 1st° AVB Right Axis Deviation Early R-Wave Progression73 y/o Male RBBB STE-Mimics
94. 94. Rate: 71 Normal Sinus - 1st° AVB Right Axis Deviation Early R-Wave Progression73 y/o Male RBBB STE-Mimics
95. 95. Rate: 71 Normal Sinus - 1st° AVB Right Axis Deviation Early R-Wave Progression 73 y/o Male RBBBIschemia, Injury, Infarct
96. 96. Rate: 71 Normal Sinus - 1st° AVB Right Axis Deviation Early R-Wave Progression 73 y/o Male RBBBIschemia, Injury, Infarct
97. 97. Rate: 71 Normal Sinus - 1st° AVB Right Axis Deviation Early R-Wave Progression73 y/o Male RBBB
98. 98. Rate: 71 Normal Sinus - 1st° AVB Right Axis Deviation Early R-Wave Progression 73 y/o Male RBBB Antero-Septal Infarct Ischemia, Injury, InfarctB
99. 99. 76 y/o FemaleShortness of Breath
100. 100. 76 y/o Female Rate & Rhythm
101. 101. 76 y/o Female Rate & Rhythm1 2 3 4 5 6
102. 102. 76 y/o Female Rate & Rhythm1 2 3 4 5 6 7 8 9 10 11 12 13
103. 103. 76 y/o Female Rate & Rhythm1 2 3 4 5 6 7 8 9 10 11 12 13 13 x 10 = 130
104. 104. Rate: 133 Sinus Tachycardia76 y/o Female Axis
105. 105. Rate: 133 Sinus Tachycardia 76 y/o Female Axis Lead I aVFNormal Positive (+) Positive (+) RAD Negative (-) Positive (+) LAD Positive (+) Negative (-)ERAD Negative (-) Negative (-)
106. 106. Rate: 133 Sinus Tachycardia Normal Axis76 y/o Female Axis
107. 107. Rate: 133 Sinus Tachycardia Normal Axis 76 y/o FemaleIntervals & Morphology
108. 108. Rate: 133 Sinus Tachycardia Normal Axis 76 y/o FemaleIntervals & Morphology
109. 109. Rate: 133 Sinus Tachycardia Normal Axis76 y/o Female STE-Mimics
110. 110. Rate: 133 Sinus Tachycardia Normal Axis 76 y/o Female STE-MimicsE - Electrolytes (hyperkalemia)L - LBBBE - Early repolarizationV - Ventricular hypertrophy (LVH)A - AneurysmT - Treatment (e.i. pericardiocentesis)I - Injury (AMI, contusion)O - Osborne waves (hypothermia)N - Non-occlusive vasospasm
111. 111. Rate: 133 Sinus Tachycardia Normal Axis 76 y/o FemaleIschemia, Injury, Infarct
112. 112. Rate: 133 Sinus Tachycardia Normal Axis76 y/o Female
113. 113. Rate: 133 Sinus Tachycardia Normal Axis Infero-Posterior & Lateral MI 76 y/o Female Ischemia, Injury, InfarctB
114. 114. Lesson 6• This concludes the course• Questions or feedback? – Paramedicine101@gmail.com