1. Basics of EKG Interpretation
Michael Rochon-Duck
July 6, 2015
Slideset adapted from:
Jennifer Ballard-Hernandez, DNP

2. Goals Understand the normal electrical activation of the heart
Correlate the ECG to the timing and direction of cardiac electrical activity
Gain confidence with recognizing common ECG findings
Start interpreting ECGs

3. What is an ECG?
Noninvasive test that examines the electrical conduction of the heart
Measures the amount of electrical voltage generated by depolarization of the heart muscle
Sum of all electrical forces (vectors) at a given moment in time
Voltage may be a negative of positive value

4. 12 Leads = 12 Vantage Points

5. Limb Leads: Vertical Plane

6. Precordial Leads: Horizontal Plane

7. Munshi 2012

9. Impulse Conduction & the ECG
Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers

10. The “PQRST” P wave - Atrial depolarization
QRS - Ventricular depolarization
T wave - Ventricular repolarization

11. The ECG Paper Horizontally Vertically One small box - 0.04 sec.
One large box sec.
Vertically
One large box mV

12. You Must Have a Method to Your Madness!
To eliminate potential errors and avoid missed data – you MUST have a protocol in your interpretation of ECG’s
The protocol must be easy, logical and sequential

13. ECG Analysis Step 1: Rate Step 2: Rhythm Step 3: Intervals-PR
Step 4: Intervals-QRS
Step 5: Axis
Step 6: ST Segment / Waves
Step 7: Overall Interpretation

14. Step 1: Calculate Rate Option 1 Interpretation? 11 x 6 = 66 bpm
Count the # of R waves in a 10 second rhythm strip, then multiply by 6.
This method should be used for all irregular rhythms
Interpretation?
11 x 6 = 66 bpm

15. Step 1: Calculate Rate Option 2 R wave
Find a R wave that lands on a bold line.
Count the # of large boxes to the next R wave. If the second R wave is 1 large box away the rate is 300, 2 boxes - 150, 3 boxes - 100, 4 boxes - 75, etc. (cont)
R wave

16. Step 1: Calculate Rate Option 2 (cont) Interpretation?
300
150
100 75 60 50
Option 2 (cont)
Memorize the sequence:
Interpretation?
Approx. 1 box less than 100 = 95 bpm

17. Step 1: Calculate Rate Option 3 (Jen’s favorite ) Interpretation?
Count the number of small boxes between two R waves and divide into 1500
Interpretation?
1500/16=93.75
HR=94

18. What is the rate?

19. What is the rate? 2

20. What is the rate? 3

21. Abnormalities in Rate >100/min = tachyarrhythmia
<60/min = bradyarrhythmia
Further defined by site of origin
Sinus node
Atrial
Junctional
Ventricular

22. The Fastest Pacemaker Captures the Heart

23. Step 2: Determine regularity
Look at the R-R distances (using a caliper or markings on a pen or paper).
Regular (are they equidistant apart)? Occasionally irregular? Regularly irregular? Irregularly irregular?
Interpretation?
Regular

24. Step 2: Rhythm Assess the P waves
Are there P waves?
Morphology: Do P waves all look alike?
Is there one P wave before each QRS?
P waves upright in I, II, aVF?
Is the PR interval constant?
Interpretation?
Normal P waves with 1 P wave for every QRS

25. Step 3: Determine PR interval
Normal: 120 – 200 ms
(3 - 5 boxes)
Interpretation?
0.12 seconds

26. Step 4: Determine the QRS Interval
Normal: 40 – 100 ms
(1 – 2.5 boxes)
Interpretation?
0.08 seconds

27. Bundle Branch Blocks

28. Bundle Branch Blocks Turning our attention to bundle branch blocks…
Remember normal impulse conduction is
SA node 
AV node 
Bundle of His  Bundle Branches  Purkinje fibers

29. Normal Impulse Conduction
Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers

30. Bundle Branch Blocks
So, depolarization of the Bundle Branches and Purkinje fibers are seen as the QRS complex on the ECG.
Right BBB
Therefore, a conduction block of the Bundle Branches would be reflected as a change in the QRS complex.

31. Bundle Branch Blocks
With Bundle Branch Blocks you will see two changes on the ECG.
QRS complex widens (> 0.12 sec).
QRS morphology changes (varies depending on ECG lead, and if it is a right vs. left bundle branch block).

32. Bundle Branch Blocks Why does the QRS complex widen?
When the conduction pathway is blocked it will take longer for the electrical signal to pass throughout the ventricles because the impulse has to travel from cell to cell inefficiently.

34. Right Bundle Branch Blocks
What QRS morphology is characteristic?
For RBBB the wide QRS complex assumes a unique, virtually diagnostic shape (upright “rabbit ears”) in those leads overlying the right ventricle, V1. V1
“Rabbit Ears”

35. Left Bundle Branch Blocks
What QRS morphology is characteristic?
For LBBB the wide QRS complex assumes a wide predominantly downward deflection leads opposite the left ventricle, i.e., V1 and V2 (right ventricular leads) and the QRS is upright and wide in V5 and V6 (may or may not be notched)

36. Bundle Branch Block RBBB QRS > 0.12
V1 rsR’ pattern and T wave inversion
V6 widened S wave and upright T
LBBB
QRS > 0.12
V1 QS pattern
V6 notched R Wave and inverted T wave

37. What causes BBBs? Hypertension Coronary artery disease
Thickened, stiffened or weakened heart muscle (cardiomyopathy)
Infection (myocarditis) of the heart muscle
Scar tissue after heart surgery
Congenital abnormality

38. BBB Left or Right?

39. BBB Left or Right?

42. Intervals PR QRS QT Normal < .2 sec (1 large box)
> .2 sec = 1st degree AV block
Causes: ischemia, senescence, medications
QRS
Normal < .12 sec (3 small boxes)
> .12 sec = IVCD; bundle branch block
Causes: congenital, ischemia/infarct, LVH, pacemaker QT
Varies with rate
Normal < ½ R-R interval
> 450 msec (QTc) = abnormal; predisposition to ventricular arrhythmias
Causes: medications, Genetic disorders

43. Step 5: Axis
The mean direction of electrical forces in the frontal plane (limb leads) as measured from the point of zero
We like to know the QRS axis because an abnormal axis can suggest disease
Normal QRS Axis: -30 to 90

44. Axis

45. Axis: Quick and Easy 
Lead I and
Lead II

46. Left Axis Deviation
Mechanical shifts: Expiration, high diaphragm (pregnancy, ascites)
Left bundle branch block
Left anterior fascicular
Emphysema
Hyperkalemia
Wolff-Parkinson-White syndrome
Congenital heart disease: Primum ASD

47. Right Axis Deviation Normal finding in children and tall thin adults
Mechanical shifts: Inspiration
Right ventricular hypertrophy
Right bundle branch block
Left posterior fascicular block
Chronic lung disease COPD
Dextrocardia
Pulmonary embolus

48. Is the QRS axis normal in this ECG?
The QRS is positive in I and negative in II.
No, there is left axis deviation.

49. Step 6: ST Segments and waves
The ST segment is the flat isoelectric section of the ECG between the end of the S wave and start of the T wave
Myocardial ischemia tends to be a regional event
MI and injury cause a variety of changes in ST segments T waves and QRS complexes
ECG changes that are global are rarely cause by ischemia i.e.pericarditis

50. Step 6: ST Segments and waves
Questions to ask:
Is there ST segment elevation or depression?
Are the T waves inverted?
Are there pathological Q waves?

51. ST Segment

52. Waves/Complexes T Wave
Peaked: hyperkalemia, hypocalcemia, hyperacute MI
Flat
w/ U wave – hypokalemia
w/o U wave –ischemia (if 2 or more contiguous leads)
Inverted
Symmetric: more likely to be ischemia (if 2 or more contiguous leads)
Assymetric: drugs, strain (LVH/subendocardial strain)
Biphasic
Ischemia (if 2 or more contiguous leads)

53. ST Elevation Infarction
The ECG changes seen with a ST elevation infarction are:
Before injury
Normal ECG
Ischemia
ST depression, peaked T-waves, then T-wave inversion
Infarction
ST elevation & appearance of Q-waves
Fibrosis
ST segments and T-waves return to normal, but Q-waves persist

54. ST Elevation Infarction
Here’s a diagram depicting an evolving infarction:
A. Normal ECG prior to MI
B. Ischemia from coronary artery occlusion results in ST depression (not shown) and peaked T-waves
C. Infarction from ongoing ischemia results in marked ST elevation
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

55. ST Segment Significant Elevation Depression
> 1mm above or below isoelectric
2 or more contiguous leads
Elevation
Infarct
*Exception: Global ST elevation in pericarditis
Depression
Ischemia
Drug effect
Electrolytes

56. Contiguous Leads Inferior Lateral Anterior Septal Posterior
II, III, aVF
Lateral
I, aVL
V5, V6
Anterior
V1-V4
Septal
V2, V3
Posterior
V1, V2, V3

57. Contiguous Leads

58. ST Segment Depression

59. ST Elevation
One way to diagnose an acute MI is to look for elevation of the ST segment.

60. ST Elevation (cont)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction.

61. Locating Myocardial Damage
Remember that the 12-leads of the ECG look at different portions of the heart. The limb and augmented leads “see” electrical activity moving inferiorly (II, III and aVF), to the left (I, aVL) and to the right (aVR). Whereas, the precordial leads “see” electrical activity in the posterior to anterior direction.
Limb Leads
Augmented Leads
Precordial Leads

62. The 12-Leads The 12-leads include: 3 Limb leads (I, II, III)
3 Augmented leads (aVR, aVL, aVF)
6 Precordial leads (V1- V6)

63. Views of the Heart Lateral portion of the heart
Some leads get a good view of the:
Anterior portion of the heart
Inferior portion of the heart

64. Anterior MI
The anterior portion of the heart is best viewed using leads V1- V4.
Left Coronary Artery
Limb Leads
Augmented Leads
Precordial Leads

65. Lateral MI
The Lateral wall of the heart is best viewed using leads Leads I, aVL, and V5- V6
Circumflex Artery
Limb Leads
Augmented Leads
Precordial Leads

66. Inferior MI
The Inferior wall of the heart is best viewed using leads Leads II, III and aVF
Right Coronary Artery
Limb Leads
Augmented Leads
Precordial Leads

67. Q Waves Q wave Late evolving or chronic stage of myocardial infarction
Significance
> 1 small box wide
> ¼ of R wave height
2 or more contiguous leads

69. Putting it all Together
Do you think this person is having a myocardial infarction. If so, where?

70. Interpretation
Yes, this person is having an acute anterior wall myocardial infarction.

71. Putting it all Together
Now, where do you think this person is having a myocardial infarction?

72. Inferior Wall MI
This is an inferior MI. Note the ST elevation in leads II, III and aVF.

73. Putting it all Together
How about now?

74. Anterolateral MI
This person’s MI involves both the anterior wall (V2-V4) and the lateral wall (V5-V6, I, and aVL)!

75. Diagnosing a MI
To diagnose a myocardial infarction you need to go beyond looking at a rhythm strip and obtain a 12-Lead ECG.
12-Lead ECG
Rhythm Strip

76. Left Ventricular Hypertrophy

77. Left Ventricular Hypertrophy
Compare these two 12-lead ECGs. What stands out as different with the second one?
The QRS complexes are very tall (increased voltage)
Normal
Left Ventricular Hypertrophy
Answer:

78. Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes?
Increased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage.
LVH
ECHOcardiogram

79. Left Ventricular Hypertrophy
Specific criteria exists to diagnose LVH using a 12-lead ECG.
For example:
The R wave in V5 or V6 plus the S wave in V1 or V2 exceeds 35 mm.

80. Now that we have the basics down
Lets do some rhythm strip analysis!

81. Sinus Rhythms
Sinus Bradycardia
Sinus Tachycardia

82. Rhythm #1 Rate? 30 bpm Regularity? regular P waves? normal
PR interval?
0.12 s
QRS duration?
0.10 s
Interpretation?
Sinus Bradycardia

83. Sinus Bradycardia
Deviation from NSR
- Rate < 60 bpm

84. Sinus Bradycardia
Etiology: SA node is depolarizing slower than normal, impulse is conducted normally (i.e. normal PR and QRS interval).

85. Rhythm #2 Rate? 130 bpm Regularity? regular P waves? normal
PR interval?
0.16 s
QRS duration?
0.08 s
Interpretation?
Sinus Tachycardia

86. Sinus Tachycardia
Deviation from NSR
- Rate > 100 bpm

87. Sinus Tachycardia
Etiology: SA node is depolarizing faster than normal, impulse is conducted normally.
Remember: sinus tachycardia is a response to physical or psychological stress, not a primary arrhythmia.

88. Premature Beats Premature Atrial Contractions (PACs)
Premature Ventricular Contractions (PVCs)

89. Rhythm #3 Rate? 70 bpm Regularity? occasionally irreg. P waves?
2/7 different contour
PR interval?
0.14 s (except 2/7)
QRS duration?
0.08 s
Interpretation?
NSR with Premature Atrial Contractions

90. Premature Atrial Contractions
Deviation from NSR
These ectopic beats originate in the atria (but not in the SA node), therefore the contour of the P wave, the PR interval, and the timing are different than a normally generated pulse from the SA node.

91. Premature Atrial Contractions
Etiology: Excitation of an atrial cell forms an impulse that is then conducted normally through the AV node and ventricles.

92. Teaching Moment
When an impulse originates anywhere in the atria (SA node, atrial cells, AV node) and then is conducted normally through the ventricles, the QRS will be narrow ( s).

93. Rhythm #4 Rate? 60 bpm Regularity? occasionally irreg. P waves?
none for 7th QRS
PR interval?
0.14 s
QRS duration?
0.08 s (7th wide)
Interpretation?
Sinus Rhythm with 1 PVC

94. PVCs Deviation from NSR
Ectopic beats originate in the ventricles resulting in wide and bizarre QRS complexes.
When there are more than 1 premature beats and look alike, they are called “uniform”. When they look different, they are called “multiform”.

95. PVCs
Etiology: One or more ventricular cells are depolarizing and the impulses are abnormally conducting through the ventricles.

96. Teaching Moment
When an impulse originates in a ventricle, conduction through the ventricles will be inefficient and the QRS will be wide and bizarre.

97. Ventricular Conduction
Normal
Signal moves rapidly through the ventricles
Abnormal
Signal moves slowly through the ventricles

98. Rhythm #5 Rate? 110 bpm Regularity? P waves? none PR interval?
Irregularly irregular
P waves?
none
PR interval?
Unable to determine
QRS duration?
0.08 s
Interpretation?
Afib

99. Rhythm #6 Rate? 90 bpm Regularity? Regular P waves? none PR interval?
Unable to determine
QRS duration?
0.08 s
Interpretation?
Aflutter

100. AV Nodal Blocks 1st Degree AV Block 2nd Degree AV Block, Type I
2nd Degree AV Block, Type II
3rd Degree AV Block

101. Rhythm #7 Rate? 60 bpm Regularity? regular P waves? normal
PR interval?
0.36 s
QRS duration?
0.08 s
Interpretation?
1st Degree AV Block

102. 1st Degree AV Block
Deviation from NSR
PR Interval > 0.20 s

103. 1st Degree AV Block
Etiology: Prolonged conduction delay in the AV node or Bundle of His.

104. Rhythm #8 Rate? 50 bpm Regularity? regularly irregular P waves?
nl, but 4th no QRS
PR interval?
lengthens
QRS duration?
0.08 s
Interpretation?
2nd Degree AV Block, Type I

105. 2nd Degree AV Block, Type I
Deviation from NSR
PR interval progressively lengthens, then the impulse is completely blocked (P wave not followed by QRS).

106. 2nd Degree AV Block, Type I
Etiology: Each successive atrial impulse encounters a longer and longer delay in the AV node until one impulse (usually the 3rd or 4th) fails to make it through the AV node.

107. Rhythm #9 Rate? 40 bpm Regularity? regular P waves? nl, 2 of 3 no QRS
PR interval?
0.14 s
QRS duration?
0.08 s
Interpretation?
2nd Degree AV Block, Type II

108. 2nd Degree AV Block, Type II
Deviation from NSR
Occasional P waves are completely blocked (P wave not followed by QRS).

109. 2nd Degree AV Block, Type II
Etiology: Conduction is all or nothing (no prolongation of PR interval); typically block occurs in the Bundle of His.

110. Rhythm #10 Rate? 40 bpm Regularity? regular P waves?
no relation to QRS
PR interval?
none
QRS duration?
wide (> 0.12 s)
Interpretation?
3rd Degree AV Block

111. 3rd Degree AV Block Deviation from NSR
The P waves are completely blocked in the AV junction; QRS complexes originate independently from below the junction.

112. 3rd Degree AV Block
Etiology: There is complete block of conduction in the AV junction, so the atria and ventricles form impulses independently of each other. Without impulses from the atria, the ventricles own intrinsic pacemaker kicks in at around beats/minute.

113. Remember
When an impulse originates in a ventricle, conduction through the ventricles will be inefficient and the QRS will be wide and bizarre.

114. VT

115. VF

116. Summary of Arrhythmias & Blocks Supraventricular
Atrial
Sinus Tach (>100)
Sinus Brady (<60)
Sinus Arrest
PAC
Atrial Tach ( )
Atrial Flutter ( )
Atrial Fib
Wandering Atrial Pacemaker
Multifocal Atrial Tachycardia
AV Nodal
PSVT
Blocks
1st Degree
2nd Degree
Mobitz I (Wenchebach)
Mobitz II
3rd Degree
Junctional
Junctional Escape (40-60)
Accelerated Junctional

117. Summary of Arrhythmias & Blocks Ventricular
PVC
V Tach
Unifocal
Multifocal (Torsade de Pointe)
V Fib
Idioventricular Rhythm (20-40)
Blocks
Left Bundle Branch
Left anterior fascicular block
Left posterior fascicular block
Right Bundle Branch

118. ECG Case Studies

119. 56 y.o. male here for preop clearance for TKR. Hx of HTN

120. 23 y.o. female presents with “racing heart”

121. 72 y.o. male presents with dizziness

122. 80 y.o. female presents with SOB and fatigue
A flutter
Left axis deviation

123. 46 y.o male presents with sternal CP

124. 65 y.o. male with diabetes presents with nausea, abdominal pain

125. 65M with asystolic cardiac arrest with Epi, bicarb, and chest compressions. He was in shock
Hyperkalemia, pH 6.6, post code

126. 45M admitted with on-and-off chest pain

127. 29F from Jamaica with sharp constant chest pain