1. Essentials of 12-Lead ECG
Interpretation
HeartStart Skills Learning Center
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2. Topics
 12-Lead ECG Overview
 Critical Concepts of Acute Coronary Syndrome
 Monitoring versus Diagnostic
 Acquisition and Transmission
 Axis Determination
 Waveform Analysis

3. Topics
 Injury, Ischemia or Infarction
 Localization of Injury
 Bundle Branch Blocks and Hemiblocks
 ST Imposters
 Differential Diagnosis of Wide Complex Tachycardias

4. What is the purpose of 12-Lead
ECGs?
• Demonstrated Advantages
– Rapid Identification of Infarction/Injury
• Diagnosis made sooner in many cases
– Decreased Time to Reperfusion Treatment
• Speeds preparation of & time to reperfusion therapies
– Increased Index of Suspicion
• Lowers false-negatives and false-positives
– Modification to Therapies
• From less invasive (Fibrinolytic) to aggressive (CABG) interventions

5. Critical Concepts in
ACS
• Ischemia
– lack of oxygenation
– ST segment depression or T wave inversion
• Injury
– prolonged ischemia
– ST segment elevation
• Infarct
– prolonged injury results in death of tissue
– may or may not show Q wave

6. Critical Concepts in ACS
 ST elevation - the key to the acute reperfusion
therapy subset
 You can’t see ST elevation without a 12-lead ECG
 Perform on every patient suspected of ACS
 Obtain early
 Repeat frequently

7. Critical Concepts in
ACS

8. Critical Concepts in ACS

9. Critical Concepts in
ACS
Acute Reperfusion Therapies
 Fibrinolytics  Percutaneous Transluminal Coronary
 Retaplase (rPA) Angioplasty (PTCA)
 Actiplase (tPA)  Balloon angioplasty
 Streptokinase (rarely used  Stent placement
today)  Atherectomy

10. Critical Concepts in ACS
 Pain is Injury
 Pain-Free is the Goal
 Time is Muscle
 Door to Reperfusion Therapy
“Time is the Tissue”

11. Monitoring vs Diagnostic
ECGs
 Extra wires
 3 wires versus 5 wires
• Monitoring Quality 12-Lead ECG
– Designed to provide information needed to determine
rate and underlying rhythm
– Designed to “filter out” artifact
• Reduces the amount and degree of electrical activity seen by
the ECG monitor

12. Monitoring vs. Diagnostic ECGs
Monitor Quality

13. Monitoring vs. Diagnostic
ECGs
• Diagnostic Quality ECG
– Designed to accurately reproduce QRS, ST and T waveforms
– Designed to look more broadly at the cardiac electrical activity
– Unfortunately, may result in greater artifact being visible

14. Monitoring vs. Diagnostic
ECGs
Diagnostic Quality

15. Monitoring vs. Diagnostic
ECGs
 Frequency Response
 Term used to describe the breadth of the electrical spectrum
viewed by the ECG monitor
 Diagnostic quality is usually 0.05 Hz to 150 Hz
 Monitor quality is usually 0.5 Hz to 20-50 Hz
 Usually printed on the ECG recording strip

16. Monitoring vs. Diagnostic
ECGs

17. Monitoring vs. Diagnostic
ECGs

18. Acquisition & Transmission
 ECG quality begins with skin preparation and electrodes
Hair removal
Skin preparation
Age & Quality of Electrodes & Cables
Electrode Placement

19. Acquisition &
Transmission
 Hair Removal
 Clipper over razor
Lessens risk of cuts
Quicker
Disposable blade clippers

20. Acquisition & Transmission

21. Acquisition &
Transmission
Skin Preparation
 Helps obtain a strong signal
 When measured from skin, heart’s electrical signal about
0.0001 - 0.003 volts
 Skin oils reduce adhesion of electrode and hinder
penetration of electrode gel
 Dead, dried skin cells do not conduct well

22. Acquisition & Transmission
 Other causes of artifact
 Patient movement
 Cable movement
- Electromagnetic Interference (EMI)

23. Acquisition &
Transmission
 Patient Movement
 Make patient as comfortable as possible
Supine preferred
 Look for subtle movement
toe tapping, shivering
 Look for muscle tension
hand grasping rail, head raised to “watch”

24. Acquisition & Transmission
 Cable Movement
 Enough “slack” in cables to avoid tugging on the
electrodes
 Many cables have clip that can attach to patient’s clothes
or bed sheet

25. Acquisition & Transmission
• Electromagnetic Interference (EMI)
– Can interfere with electronic equipment
– 60 cycle interference is a type of EMI
– Look for nearby cell phones, radios or electrical devices
– No contact between cables & power cords
– Turn off or move away from AC devices
– Use shielded cables; inspect for cracks

26. Acquisition & Transmission
 Things to look for
 Little or no artifact
 Steady baseline

27. Acquisition & Transmission

28. Acquisition & Transmission
 ECG Accuracy depends upon
 Lead placement
 Frequency response
 Calibration
 Paper speed

29. Limb Lead Placement

30. Chest Lead Placement
V1: 4th ICS right of sternum
V2: 4th ICS left of sternum
V3: between leads V2 and V4
V4: 5th left midclavicular line
V5: level with V4 at left anterior
axillary line
V6: level with V5 at left midaxillary
line

31. Chest Lead Placement

32. ECG Accuracy
Look for:
 Negative aVR
 if aVR upright, look for reversed leads
 One complete cardiac cycle in each lead
 Diagnostic frequency response
 Proper calibration
 Appropriate speed

33. ECG Accuracy
 Frequency Response
 Display screen is non-diagnostic
 Use the printed ECG for ST segment analysis

34. ECG Accuracy
Calibration
 Voltage measured vertically
 Each 1 mm box = 0.1 mV
 1 mV = 10 mm
calibration standard
 Confirm calibration
calibration impulse should be 10 mm (2 big boxes tall)
stated calibration should be “x 1.0”

35. Calibration
Calibration

36. ECG Accuracy
 Paper Speed
 Standard is 25 mm/sec
Faster paper speed means the rhythm will appear slower and
the QRS wider
Slower paper speed means the rhythm will appear faster and
the QRS narrower

37. Paper Speed
Paper Speed

38. Time Differences

39. When to
Acquire
Assessment Treatment
Vital Signs Oxygen
Oxygen Saturation Aspirin
IV Access Nitroglycerin
12-Lead ECG Morphine
Brief History
Modified from “The Ischemic Chest Pain Algorithm”, ACLS Textbook, American Heart Association, 2005.

40. Exposing the Chest
Immediately upon suspecting ACS...
Remove all clothing above the waist
Or, open shirt/blouse
Replace with gown (if possible)
Allows for complete exam
Minimizes wire entanglement
Enhances quick defibrillation if VF occurs

41. Essentials of 12 Lead
ECG Interpretation
Topics Discussed:
1. Anatomy Revisited
2. The 12 Lead ECG Device
3. The 12 Lead ECG Format
4. Waveform Components
5. Lead Views

42. Anatomy Revisited
 RCA
 Right Ventricle
 Inferior wall of LV
 Posterior wall of LV (75%)
 SA Node (60%)
 AV Node (>80%)
 LCA
 Septal wall of LV
 Anterior wall of LV
 Lateral wall of LV
 Posterior wall of LV (10%)

43. Anatomy Revisited
 SA node
 Intra-atrial pathways
 AV node
 Bundle of His
 Left and Right
bundle branches
 left anterior fascicle
 left posterior fascicle
 Purkinje fibers

44. The 12 Lead ECG Device
 Device serves as a voltmeter
 Measures the flow of electricity
 Unipolar versus Bipolar Leads

45. Bipolar Leads
• 1 (+) and 1 (-) electrode
– RA always (-)
– LL always (+)
– LA both (+) & (-)
• Traditional Limb Leads
are examples of these
– Lead I
– Lead II
– Lead III
• View from a vertical
plane

46. Unipolar Leads
 1 positive electrode & 1
negative “reference point”
 calculated by using summation
of 2 negative leads
 Augmented Limb Leads
 aVR, aVF, aVL
 view from a vertical plane
 Precordial or Chest Leads
 V1-V6
 view from a horizontal plane

47. The 12-Lead ECG Format

48. The 12-Lead ECG Format
Device prints out 2.5 sec
each of Leads I, II, III then
switches to aVR, aVL, aVF
then switches to V1, V2,
V3 and then to V4, V5,
V6 (varies by device)
Device computer
analyzes all 10 sec of all
12 leads but only prints
2.5 sec of each group

49. The 12-Lead ECG Format
Not always
accurate
The computer IS
very accurate at
measuring
intervals &
durations

50. Waveform Components:
R Wave
First positive
deflection; R wave
includes the
downstroke returning
to the baseline

51. Waveform Components:
Q Wave
First negative
deflection before R
wave;
Q wave includes
the negative
downstroke &
return to baseline

52. Waveform Components:
S Wave
Negative deflection
following the R
wave; S wave
includes departure
from & return to
baseline

53. Waveform Components:
QRS
 Q waves
 Can occur normally in several leads
Normal Q waves called physiologic
 Physiologic Q waves
< .04 sec (40ms)
 Pathologic Q
>.04 sec (40 ms)

54. Waveform Components:
QRS
 Q wave
 Measure width
 Pathologic if greater than or equal to 0.04 seconds (1 small box)

55. Waveform Components:
QS Complex
Entire complex is
negatively deflected; No R
wave present

56. Waveform Components:
J-Point
Junction between end of QRS
and beginning of ST segment;
Where QRS stops & makes a
sudden sharp change of
direction

57. Waveform Components:
ST Segment
Segment between J-point and
beginning of T wave

58. Waveform Components:
ST Segment
• Need reference point
– Compare to TP segment
– DO NOT use PR segment as reference!

59. Waveform Components:
Practice
 Find J-points and ST segments

60. Lead “Views”

61. 12-Lead Groups
I AVR V1 V4
II AVL V2 V5
III AVF V3 V6
Limb Leads Chest Leads

62. Inferior Wall
 II, III, aVF
 View from Left Leg ⊕
 inferior wall of left ventricle
I AVR V1 V4
II AVL V2 V5
III AVF V3 V6

63. Inferior Wall
Posterior View
– Portion resting on diaphragm
– ST elevation suspect inferior
injury
I AVR V1 V4
II AVL V2 V5
III AVF V3 V6 Inferior Wall

64. Lateral Wall
I, aVL
– View from Left Arm ⊕
– Lateral wall of left ventricle
I AVR V1 V4
II AVL V2 V5
III AVF V3 V6

65. Lateral Wall
V5, V6
– Left lateral chest
– Lateral wall of left ventricle
I AVR V1 V4
II AVL V2 V5
III AVF V3 V6

66. Lateral Wall
I, aVL, V5, V6
– ST elevation at suspect
lateral wall injury
I AVR V1 V4
II AVL V2 V5
Anterior View
III AVF V3 V6
Posterior View

67. Anterior Wall
V3, V4
– Left anterior chest
– ⊕ electrode on anterior chest
I AVR V1 V4
II AVL V2 V5
III AVF V3 V6

68. Anterior Wall
V3, V4
– ST segment elevation with
suspect anterior wall injury
I AVR V1 V4
II AVL V2 V5
III AVF V3 V6

69. Septal Wall
V1, V2
• Along sternal borders
• Look through right ventricle & see
septal wall
I AVR V1 V4
II AVL V2 V5
III AVF V3 V6

70. Septal
V1, V2
• Septum is left ventricular tissue
I AVR V1 V4
II AVL V2 V5
III AVF V3 V6

71. ST Segment
Analysis
ST segment deviation 1 mm or more from the baseline

72. 12-Lead ECG
AMI recognition
Two things to know
What to look for
Where you are looking

73. AMI Recognition
What to look for
 ST segment elevation
One millimeter or more (one small box)
Present in two anatomically contiguous leads

75. Axis Determination & Deviation
 Why Axis Determination?
 Definitions
 Axis Quadrants
 Axis Determination
 Axis Deviation
 Physiologic vs Pathologic

76. Axis Determination & Deviation
 Why Axis Determination?
 The ability to identify hemiblocks (“fascicular blocks”) is the main
reason you need to be able to determine axis

77. Axis Determination & Deviation
“It is my opinion that the inability to determine the presence
of a hemiblock has often been the cause of complete heart
block when well-intentioned caregivers have improperly
administered Lidocaine.”
Mike Taigman, “Taigman’s Advanced Cardiology”, Brady, 1995, p. 71

78. Axis Determination & Deviation
 What is Axis?
 “the general (mean vector) direction of electrical impulses as they
travel through the heart”
 “the sum total of all electrical currents generated by the ventricular
myocardium during depolarization”
 normally from upper right to lower left

79. Axis Determination & Deviation
 What do you need to determine the axis of an ECG?
 The 12 Lead ECG
 Leads CORRECTLY placed on the patient
RA on the right arm
LA on the left arm
LL on the left leg
Not on the chest or abdomen
 Knowledge of axis deviation

80. Axis Reference
• Hexaxial Reference System
• The six frontal leads create
six poles that intersect at
the center of the heart
• Each pole has a positive &
negative axis
• Each + and - end is
assigned a value expressed
in degrees
• Hexaxial then divided into
quadrants (easier to use)

81. Axis Quadrants
Left axis -90°
-30 to -90 ° +120° -60°
aVL
Normal axis aVR
No LAD -30°
-30 to 90° -150°
Man’s
Land
Right axis +180° 0° I
90 to 180°
RAD Normal
+150° +30°
Extreme Right axis or
“No Man’s Land” +120° +60°
-90 to 180° III +90° II
aVF

82. Axis Determination
Quick Axis Determination
 Determine the net QRS deflection in Leads I and aVF (positive or
negative)
Lead I aVF
Normal axis
LAD
RAD
ERAD

83. Axis Determination
Estimating Axis Quickly
Determine the net QRS deflection in leads I and aVF (-/+)
If the net QRS in Lead I is nearly the same as aVF, then axis midway
between or 45°
 We estimate by calling it, “between +40° and +50°
If the net QRS in Lead I is positive and is obviously greater than aVF,
then axis closer to lead I
 Estimate as “Between 0° and 40°”
If the net QRS in aVF is positive and greater than Lead I, then axis is
+50° and +90°

84. Axis Deviation
Pathologic versus Physiologic LAD
1. First step
a) Do I have LAD?
b) If yes, then proceed on
2. Look at Lead II
a) If the net QRS deflection is more negative than
positive, then the axis must be MORE NEGATIVE
than -30°

86. Ischemia, Injury & Infarction
Definitions
Injury/Infarct Recognition
Localization & Evolution
Reciprocal Changes
The High Acuity Patient

87. The Three I’s
 Ischemia
 lack of oxygenation
 ST segment depression or T wave inversion
 Injury
 prolonged ischemia
 ST segment elevation
 Infarct
 death of tissue
 may or may not show a Q wave

88. Injury/Infarct Recognition
Well Perfused Myocardium
Epicardial Coronary Artery
Septum
Lateral Wall of LV
Positive Electrode
Interior Wall of LV

89. Injury/Infarct Recognition
Normal ECG

90. Injury/Infarct Recognition
Ischemia
Epicardial Coronary Artery
Septum Left Lateral Wall of LV
Ventricular
Cavity
Positive Electrode
Interior Wall of LV

91. Injury/Infarct Recognition
 Ischemia
 Inadequate oxygen to tissue
 Represented by ST depression or T inversion
 May or may not result in infarct or Q waves

92. Injury/Infarct Recognition
ST Segment Depression

93. Injury/Infarct Recognition
Thrombus
Injury
Ischemia

94. Injury/Infarct Recognition
Thrombus
Ischemia

95. Injury/Infarct Recognition
 Injury
 Prolonged ischemia
 Represented by ST elevation
referred to as an “injury pattern”
 Usually results in infarct
may or may not develop Q wave

96. Injury/Infarct Recognition
ST Segment Elevation

97. Injury/Infarct Recognition
Thrombus
Infarcted Area
Electrically Silent
Ischemia
Depolarization

98. Injury/Infarct Recognition
 Infarct
 Death of tissue
 Represented by Q wave
 Not all infarcts develop Q waves

99. Injury/Infarct Recognition
Q Waves

100. Injury/Infarct Recognition
Thrombus
Infarcted Area
Electrically Silent
Ischemia
Depolarization

101. Injury/Infarct Recognition
ST segment
elevation
Present in two or
more
anatomically
contiguous
leads

102. Injury/Infarct Recognition: Practice

103. Localization
I AVR V1 V4 Inferior: II, III, AVF
II AVL V2 V5 Septal: V1, V2
Anterior: V3, V4
III AVF V3 V6 Lateral: I, AVL, V5, V6

104. 12-Lead Localization
I Lateral AVR V1 Septal V4 Anterior
II Inferior AVL Lateral V2 Septal V5 Lateral
III Inferior AVF Inferior V3 Anterior V6 Lateral

105. Localization: Left Coronary Artery (LCA)
 Left Main (proximal LCA) occlusion
 Extensive Anterior injury
 Left Circumflex (LCX) occlusion
 Lateral injury
 Left Anterior Descending (LAD) occlusion
 Anteroseptal injury

106. Localization Practice ECG

107. Localization Practice ECG

108. Localization Practice ECG

109. Localization: Extensive Anterior MI
 Evidence in septal, anterior, and lateral leads
 Often from proximal LCA lesion
 “Widow Maker”
 Complications common
 Left ventricular failure
 CHF / Pulmonary Edema
 Cardiogenic Shock

110. Localization: Definitive Therapy for
Extensive AWMI
 Normal blood pressure
 Thrombolysis may be indicated
 Signs of shock
 PTCA
 CABG

111. Localization: LCA Occlusions
 Other considerations
 Bundle branches supplied by LCA
 Serious infranodal heart block may occur

112. Localization: Right Coronary Artery (RCA)
 Proximal RCA occlusion
 Right Ventricle injured
 Posterior wall of left ventricle injured
 Inferior wall of left ventricle injured
 Posterior descending artery (PDA) occlusion
 Inferior wall of right ventricle injured

113. Localization Practice ECG

114. Localization: Proximal RCA Occlusion
 Right Ventricular Infarct (RVI)
 12-lead ECG does not view right ventricle
 Use additional leads
V3R - V6R
V4R
 Right precordial leads
same anatomical landmarks as on left for V3 - V6 but placed on the right
side

115. Localization Practice ECG
Note: “R” designation manually placed on
this ECG for teaching purposes

116. Localization: ECG Evidence of RVI
 Inferior MI (always suspect RVI)
 Look for ST elevation in right-sided V leads (V3-V6)

117. Localization: Physical Evidence of RVI
 Dyspnea with clear lungs
 Jugular vein distension
 Hypotension
 Relative or absolute

118. Localization: Treatment for RVI
 Use caution with vasodilators
 Small incremental doses of MS
 NTG by drip
 Treat hypotension with fluid
 One to two liters may be required
 Large bore IV lines

119. Localization: Posterior Wall MI (PWMI)
 Usually extension of an inferior or lateral MI
 Posterior wall receives blood from RCA & LCA
 Common with proximal RCA occlusions
 Occurs with LCX occlusions
 Identified by reciprocal changes in V1-V4
 May also use Posterior leads to identify
V7: posterior axillary line level with V6
V8: mid-scapular line level with V6
V9: left para-vertebral level with V6

120. Localization Practice ECG

121. Localization: Left Coronary Dominance
 Approximately 10% of population
 LCX connects to posterior descending artery and dominates inferior wall
perfusion
 In these cases when LCX is occluded, lateral and inferior walls infarct
 Inferolateral MI

122. Localization Practice ECG

123. Localization Summary
 Left Coronary Artery
 Septal
 Anterior
 Lateral
 Possibly Inferior
 Right Coronary Artery
 Inferior
 Right Ventricular Infarct
 Posterior

124. Evolution of AMI
• Hyperacute
– Early change suggestive of AMI
– Tall & Peaked
– May precede clinical symptoms
– Only seen in leads looking at
infarcting area
– Not used as a diagnostic finding

125. Evolution of AMI
 Acute
 ST segment elevation
 Implies myocardial injury
occurring
 Elevated ST segment presumed
acute rather than old

126. Evolution of AMI
• Acute
– ST segment Elevated
– Q wave at least 40 ms
wide = pathologic
– Q wave associated with
some cellular necrosis

127. Evolution of AMI
 Age Undetermined
 Wide (pathologic) Q wave
 No ST segment elevation
 Old or “age undetermined” MI

128. AMI Recognition
A normal 12-lead ECG DOES NOT
mean the patient is not having acute
ischemia, injury or infarction!!!

129. Practice

130. Practice

131. Practice

132. Reciprocal Changes
+ +

133. Reciprocal Changes
II, III, AVF I, AVL, V Leads

134. Reciprocal Changes: Practice

135. Reciprocal Changes: Practice

136. AMI Recognition
 Reciprocal changes
 Not necessary to presume infarction
 Strong confirming evidence when present
 Not all AMIs result in reciprocal changes

137. Summary
 ST segment elevation is presumptive evidence for Acute
Myocardial Infarction
 Other conditions may also cause ST elevation
 Known as Imposters

138. Practice Case 1

139. Practice Case 2

141. Hemiblocks & Bundle Branch Blocks
 Value
 Help to identify patients at high risk for complete heart block
Hemiblocks, Bundle branch blocks and AV blocks are precursors to complete
heart block
 You are Alert & Better Prepared!!!

142. Anatomy Review
 Anatomy
 Bundle of His
 Left Bundle Branch
Anterior fascicle
 long, thin; only blood supply from LAD
Posterior fascicle
 shorter, thick; blood supply from RCA and LCX
 Right Bundle Branch

143. Definitions
 Hemiblock
 Also called fascicular blocks
 block in one of the two fascicles of the left bundle branch
 Bundle Branch Block
 block of the entire left or right bundle branch

144. Hemiblocks
 Posterior fascicle
 Much more difficult to have block  greater disease
 Less common but more concerning
 Supplies majority of inferior wall of LV
 If blocked, results in right axis deviation

145. Hemiblocks
 Anterior fascicle
 Easier to have block; More common
 Supplies superior wall of LV
 If blocked, results in pathologic left axis deviation

146. Hemiblock Identification
 Left Anterior Hemiblock  Left Posterior Hemiblock
 Pathologic Left Axis Deviation  Right Axis Deviation
small q wave in lead I small r wave in lead I
small r wave in lead III small q wave in lead III
 Normal QRS or RBBB  Normal QRS or RBBB
usually does have RBBB
“absence of right
ventricular hypertrophy

147. Precursors to Complete Heart Block
 Any Type II AV Block
 Anyone with disease of both bundles
 Anyone with two or more of any blocks
 Examples:
 Prolonged P-R & anterior hemiblock
 RBBB & anterior hemiblock
 RBBB & posterior hemiblock
 Prolonged P-R with anterior hemiblock & RBBB

148. Precursors to Complete Heart Block
 If recognize precursors to CHB, then:
 Have high index of suspicion for CHB
 Have TCP ready (standby mode)
 Patient may need a pacemaker
 Administration of Lidocaine and other ventricular anti-Arhythmics
may result in CHB
Lidocaine contraindicated in patients with precursors to CHB unless TCP
in place and ready

149. Bundle Branch Block (BBB)
 Can be pre-existing condition
 Can be caused by ACS
 If AMI caused
 60-70% associated with pump
failure
 40-60% mortality w/o reperfusion

150. Bundle Branch Block
Can Mimic or Hide Evidence Needed to Identify AMI
 May Produce  May Hide
 ST elevation  ST elevation
 ST depression  ST depression
 Tall T waves  Tall T waves
 Inverted T waves  Inverted T waves
 Wide Q waves  Wide Q waves

151. BBB Problem
 BBB Problem
 Critical to reperfuse patients with BBB produced by ACS
 ACS “harder” to identify on ECG when BBB present
 New or presumably new BBB is an indication for thrombolytic
therapy

152. BBB Recognition
 Fundamental Criteria
Wide QRS
> 100 ms (or, 0.10 sec)
Supraventricular rhythm

153. BBB Recognition

154. BBB Recognition

155. Normal Ventricular Conduction
 Normal Conduction
 fibers of LBB begin conduction
 impulse travels across interventricular
septum from left to right
 towards + electrode creates small r wave
 travels across ventricles causing
depolarization of both simultaneously
 LV contributes most to complex
 impulse travels away from + electrode
creates primarily negative complex

156. RBBB
 RBBB in V1
 no change in initial impulse
travel
 small r wave
 impulse depolarizes LV by
itself since RBBB
 RV depolarized by impulse
thru muscle
 it now contributes to
complex
 travels toward + electrode
creating positive deflection

157.  LBBB in V1
 initial deflection altered LBBB
since travels right to left
now
 Q wave or small q wave
 RV depolarizes
unopposed
 may produce small r
wave
 travels across septum to
depolarize LV
 deep S wave

158. BBB Recognition
Terminal Force in V1
 direction of deflection prior
to J point

159. BBB Recognition
• Use V1
• Find Terminal force
• Identify direction of terminal force
– Downward  LBBB
– Upward  RBBB
• Picture a Steering Wheel
– Right turn  turn signal goes up
– Left turn  turn signal goes down

160. BBB Recognition Practice

161. BBB Recognition Practice

163. Injury/Infarct Imposters
 Some Common Examples (not all inclusive list)
 Ventricular & Paced Rhythms
 LBBB Conditions that make the identification of acute
injury/infarction DIFFICULT or IMPOSSIBLE
 LVH
 Benign Early Repolarization
 Pericarditis

164. Injury/Infarct Imposters
Imposters can incorrectly place an ECG into any
of the three categories
ST Elevation ST Depression Normal
BBB T wave inversion Non-diagnostic

165. Ventricular & Paced Rhythms
 Can mask or mimic every ECG change suggestive of
ischemia/injury
Paced rhythms
Idioventricular rhythms
V-Tach
PVCs

166. Ventricular & Paced Rhythms

167. Differential Diagnosis of Wide Complex
Tachycardias
 Necessary for appropriate treatment
 Identify factors that favor one rhythm
 Possibilities:
 VT, SVT with aberrant conduction, Afib/Aflutter with aberrant
conduction

168. Differential Diagnosis of Wide Complex
Tachycardias
Top 10 List for Imposters
 1. Ventricular Tachycardia  6. VT
 2. Ventricular Tach  7. VT
 3. VT  8. VT
 4. VT  9. SVT with preexisting BBB
 5. VT  10. SVT with aberrant
conduction

169. Differential Diagnosis of Wide Complex
Tachycardias
Factors Favoring VT
 Concordance across all V leads (+/-)
 ERAD axis deviation (“no man’s land”)
 QRS > .14 sec
 AV dissociation
 Suggestive QRS morphology

170. Differential Diagnosis of Wide Complex
Tachycardias

171. Differential Diagnosis of
Wide Complex Tachycardias

172. Left Ventricular Hypertrophy (LVH)
 Enlarged left ventricle
 Pumping against increased resistance
 Chronic overfilling

173. LVH
May Produce May Hide
ST elevation ST elevation
ST depression ST depression
Tall T waves Tall T waves
Inverted T waves Inverted T waves

174. LVH
 Does not abnormally widen QRS
 Increases height and depth of QRS
 Recognized by this increase
 Three step recognition formula

175. LVH

176. LVH Recognition
• Step 1
– Look in V1 and V2
– Pick the deepest negative deflection (S wave)
– Count small boxes of negative deflection in that lead
– Remember that number

177. LVH Recognition

178. LVH Recognition
• Step 2
– Look in V5 and V6
– Pick the tallest positive deflection (R wave)
– Count small boxes of positive deflection
– Remember that number

179. LVH Recognition

180. LVH Recognition
• Step 3
– Add the two numbers together
– Suspect LVH if the sum is > 35 (> 35 mm)

181. LVH Recognition

182. LVH Recognition

183. Benign Early Repolarization

184. Benign Early Repolarization
 Normal variant; Difficult to identify
 Produces
 ST elevation
 Tall T waves
 Changes usually seen in anterior & lateral leads
 Most often seen in males ages 20-40
 More common in African-American males
 Thin, young persons

185. Benign Early Repolarization
 Look for notch at J-point
 ST segment and J-point create a “fish hook” appearance

186. Benign Early Repolarization

187. Pericarditis

188. Pericarditis
 May be viral, bacterial or metabolic
 Secondary to recent cardiac surgery
 Post MI
 IV Drug abuse
 Clinical presentation may include CP
 Often produces diffuse ST elevation on ECG plus clinical
presentation

189. Pericarditis
 Correlate Diffuse ST segment elevation with Clinical Presentation
 Sharp, “Stabbing” chest pain
 Can be localized
 May be relieved by movement, respiration, position, swallowing
 May radiate to base of neck, between shoulder blades

190. Pericarditis
 May produce ST elevation in any lead
 May be in all leads
 May not be anatomically grouped
 J-point notching often present
 Fish hook

191. Medications
 Some medications affect the ECG
 Digitalis
ST depression
Characteristic sag

192. Summary
 Imitators can produce ST elevation or depression
 Imitators can eliminate ST elevation or depression
 Most frequent imitators
LVH
BBB
Paced rhythms

193. Summary
 Imitators can produce ST elevation or depression
 Imitators can eliminate ST elevation or depression
 Most frequent imitators
 LVH
 BBB
 Paced rhythms

194. Summary
• If QRS is wide
– Consider BBB
– Consider ventricular rhythm (or paced)
• If QRS is narrow
– Consider LVH
– Consider pericarditis
– Consider early repolarization

195. Summary
 “Fish hooks” often seen with:
 Pericarditis
 BER
 “Fish hooks” can also be seen with ACS

196. Summary
The presence of a potential imposter
DOES NOT ALWAYS
make it impossible to identify injury/infarction