Basics of ECG Presented by- Dr. Mohammad Rehan DNB Medicine SDMH Jaipur Moderator- Dr. Madhulika Sharma HOD (General Medicine)

1. Basics of ECG
• Dr Mohammad Rehan

2. HISTORY
• 1842- Italian scientist Carlo Matteucci realizes that
electricity is associated with the heart beat
• 1876- Irish scientist Marey analyzes the electric
pattern of frog’s heart
• 1895 - William Einthoven , credited for the
invention of EKG
• 1906 - using the string electrometer EKG,
William Einthoven diagnoses some heart problems

3. CONTD…
• 1924 - the noble prize for physiology or
medicine is given to William Einthoven for his
work on EKG
• 1938 -AHA and Cardiac society of great Britan
defined and position of chest leads
• 1942- Goldberger increased Wilson’s Unipolar
lead voltage by 50% and made Augmented leads
• 2005- successful reduction in time of onset of
chest pain and PTCA by wireless transmission of
ECG on his PDA.

5. MODERN ECG
INSTRUMENT

6. WHAT IS AN
EKG?
•The electrocardiogram (EKG) is a representation
of the electrical events of the cardiac cycle.
•Each event has a distinctive waveform
•the study of waveform can lead to greater insight
into a patient’s cardiac pathophysiology.

7. WITH EKGS WE CAN
IDENTIFY
Arrhythmias
Myocardial ischemia and infarction
Pericarditis
Chamber hypertrophy
Electrolyte disturbances (i.e. hyperkalemia,
hypokalemia)
Drug toxicity (i.e. digoxin and drugs which
prolong the QT interval)

8. DEPOLARIZATION
• Contraction of any muscle is associated with
electrical changes called depolarization
• These changes can be detected by electrodes
attached to the surface of the body

9. PACEMAKERS OF THE
HEART
• SANode - Dominant pacemaker with an
intrinsic rate of 60 - 100 beats/minute.
• AVNode - Back-up pacemaker with an
intrinsic rate of 40 - 60 beats/minute.
• Ventricular cells - Back-up pacemaker with
an intrinsic rate of 20 - 45 bpm.

10. • Standard calibration
– 25 mm/s
– 0.1 mV/mm
• Electrical impulse that travels towards the electrode
produces an upright (“positive”) deflection

11. IMPULSE CONDUCTION
& THE ECG
Sinoatrial node
AVnode
Bundle of His
Bundle Branches
Purkinje fibers

12. THE “PQRST”
• P wave- Atrial depolarization
• QRS- Ventricular
depolarization
• T wave-Ventricular
repolarization

13. THE PR
INTERVAL
Atrial depolarization
+
delay in AV junction
(AVnode/Bundle of His)
(delay allows time for
the atria to contract
before the ventricles
contract)

14. NORMAL ECG

15. THE ECG
PAPER
• Horizontally
– One small box - 0.04 s
– One large box - 0.20 s
• Vertically
– One large box - 0.5 mV

16. EKG
LEADS
which measure the difference in electrical potential
between two points
1) Bipolar Leads: Two different points on the body
2) Unipolar Leads: One point on the body and a virtual
reference point with zero electrical potential, located in
the center of the heart

17. EKG
LEADS
The standard EKG has 12 leads:
3 Standard Limb Leads
3 Augmented Limb Leads
6 Precordial Leads

18. STANDARD
LIMB LEADS

19. STANDARD
LIMB LEADS

20. AUGMENTED
LIMB LEADS

21. ALL LIMB
LEADS

22. PRECORDIAL LEADS

23. PRECORDIAL LEADS

24. RIGHT SIDED & POSTERIOR
CHEST LEADS

25. ECG RULES
• Professor Chamberlains 10 rules of normal:-

26. RULE
1
PR interval should be 120to 200
milliseconds or3 to 5 little squares

27. RULE
2
The width of the QRS complex should not
exceed 110ms, less than 3 little squares

28. RULE
3
The QRS complex should be dominantly upright in
leads I and II

29. RULE
4
QRS and T waves tend to have the same
general direction in the limb leads

30. RULE
5
All waves are negative in lead aVR

31. RULE 6
The R wave must grow from V1 to at least V4
The S wave must grow from V1 to at least V3
and disappear in V6

32. RULE
7
The ST segment should start isoelectric
except in V1and V2 where it may be elevated

33. RULE
8
The P waves should be upright in I, II, and V2 to V6

34. RULE
9
There should be no Q wave or only a small q less
than 0.04 seconds in width in I, II, V2 to V6

35. RULE
10
The T wave must be upright in I, II, V2 to V6

36. P WAVE
• Alwayspositive in lead I and II
• Alwaysnegative in lead aVR
• < 3 small squares in duration
• < 2.5 small squares in amplitude
• Commonly biphasic in lead V1
• Best seen in leads II

37. RIGHT ATRIALENLARGEMENT
• Tall (> 2.5 mm), pointed P waves (P Pulmonale)

38. RIGHT ATRIAL ENLARGEMENT
– TAKE A LOOK AT THIS ECG. WHAT DO
YOU NOTICE ABOUT THE P WAVES?

39. RIGHT ATRIAL ENLARGEMENT
– To diagnose RAE you can use the following criteria:
• II
• V1 or V2
P > 2.5 mm,or
P > 1.5mm
Remember 1 small
box in height = 1 mm
A cause of RAE is RVH from pulmonary hypertension.
> 2 ½ boxes (in height)
> 1 ½ boxes (in height)

40. • Notched/bifid (‘M’shaped) P wave (P
‘mitrale’) in limb leads
LEFTATRIAL ENLARGEMENT

41. LEFT ATRIAL ENLARGEMENT
– TAKE A LOOK AT THIS ECG. WHAT DO
YOU NOTICE ABOUT THE P WAVES?
Notched
Negative deflection
The P waves in lead II are notched and in lead V1 they
have a deep and wide negative component.

42. LEFT ATRIAL ENLARGEMENT
– To diagnose LAE you can use the following criteria:
• II
• V1
> 0.04 s (1 box) between notched peaks, or
Neg. deflection > 1 box wide x 1 box deep
Normal LAE
A common cause of LAE is LVH from hypertension.

43. P Pulmonale
P Mitrale

44. VENTRICULAR
HYPERTROPHY

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

46. LEFT VENTRICULAR
HYPERTROPHY
• Criteria exists to diagnose LVH using a 12-lead ECG.
– For example:
• The R wave in V5 or V6 plus the Swave in V1 or V2
exceeds 35 mm.
• However, for now, all
you need to know is
that the QRS voltage
increases with LVH.

47. LEFT VENTRICULAR HYPERTROPHY
– TAKE A LOOK AT THIS ECG. WHAT DO YOU
NOTICE ABOUT THE AXIS AND QRS
COMPLEXES OVER THE LEFT VENTRICLE
(V5, V6) AND RIGHT VENTRICLE (V1, V2)?
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.
The deep S waves
seen in the leads over
the right ventricle are
created because the
heart is depolarizing
left, superior and
posterior (away from
leads V1, V2).

48. LEFT VENTRICULAR HYPERTROPHY
– To diagnose LVH you can use the following criteria*:
•
• avL
R in V5 (or V6) + Sin V1 (or V2) > 35 mm, or
R > 13 mm
A common cause of LVH
is hypertension.
* There are several
other criteria for the
diagnosis of LVH.
S = 13 mm
R = 25 mm

49. LEFT VENTRICULAR
HYPERTROPHY
• Sokolow &Lyon Criteria
• Sin V1+ R in V5 or V6 > 35 mm
• An R wave of 11 to 13 mm (1.1 to 1.3 mV)
or more in lead aVL is another sign of
LVH

51. RIGHT VENTRICULAR
HYPERTROPHY
– TAKE A LOOK AT THIS ECG. WHAT DO YOU
NOTICE ABOUT THE AXIS AND QRS
COMPLEXES OVER THE RIGHT VENTRICLE
(V1, V2)?
There is right axis deviation (negative in I, positive in II) and
there are tall R waves in V1, V2.

52. RIGHT VENTRICULAR HYPERTROPHY
– To diagnose RVH you can use the following criteria:
•
• V1
Right axis deviation, and
R wave > 7mm tall
A common
cause of RVH
is left heart
failure.

53. RIGHT VENTRICULAR HYPERTROPHY
– Compare the R waves in V1, V2 from a normal ECG and one from a
person with RVH.
– Notice the R wave is normally small in V1, V2 because the right ventricle
does not have a lot of muscle mass.
– But in the hypertrophied right ventricle the R wave is tall in V1, V2.
Normal RVH

54. SHORT PR INTERVAL
• WPW (Wolff-
Parkinson-White)
Syndrome
• Accessory pathway (Bundle
of Kent) allows early
activation of the ventricle
(delta wave and short PR
interval)

55. LONG PR INTERVAL
• First degree Heart Block

56. QRS COMPLEXES
• Nonpathological Q waves may present in I, III, aVL,
V5, and V6
• R wave in lead V6 is smaller than V5
• Depth of the Swave, should not exceed 30 mm
• Pathological Q wave > 2mm deep and > 1mm wideor
> 25% amplitude of the subsequent Rwave

57. QRS IN LVH & RVH

58. CONDITIONS WITH TALL R IN V1

60. RIGHT ATRIALAND VENTRICULAR
HYPERTROPHY

61. ST SEGMENT
• ST Segment is flat (isoelectric)
• Elevation or depression of ST segment by 1
mm or more
• “J” (Junction) point is the point between
QRS and ST segment

62. VARIABLE SHAPES OF ST
SEGMENT ELEVATIONS IN AMI

63. T-WAVE
• Normal T wave is asymmetrical, first half having a
gradual slope than the second
• Should be at least 1/8 but less than 2/3 of the
amplitude of the R
• T wave amplitude rarely exceeds 10 mm
• Abnormal T waves are symmetrical, tall, peaked,
biphasic or inverted.
• T wave follows the direction of the QRS deflection.

64. T-WAVE

65. QT INTERVAL
1. Total duration of Depolarization and
Repolarization
2. QT interval decreases when heart rate increases
3. For HR = 70 bpm, QT<0.40 sec.
4. QT interval should be 0.35 0.45 s,
5. Should not be more than half of the interval
between adjacent R waves (RR interval).

66. QT INTERVAL

67. U-WAVE
• U wave related to afterdepolarizations which
follow repolarization
• U waves are small, round, symmetrical and
positive in lead II, with amplitude < 2 mm
• U wave direction is the same as T wave
• More prominent at slow heart rates

68. Determining the Heart Rate
Rule of 300/1500
10 Second Rule

69. RULE OF 300
Count the number of “big boxes” between two
QRS complexes, and divide this into 300. (smaller
boxes with 1500)
for regular rhythms.

70. WHAT IS THE
HEART RATE?
(300 / 6) = 50 bpm

71. WHAT IS THE
HEART RATE?
(300 / ~ 4) = ~ 75 bpm

72. WHAT IS THE
HEART RATE?
(300 / 1.5) = 200 bpm

73. THE RULE
OF 300It may be easiest to memorize the following table:
No ofbig
boxes
Rate
1 300
2 150
3 100
4 75
5 60
6 50

74. 10 SECOND
RULE
EKGs record 10 seconds of rhythm per page,
Count the number of beats present on the EKG
Multiply by 6
For irregular rhythms.

75. WHAT IS THE
HEART RATE?
33 x 6 = 198 bpm

76. CALCULATION OF HEART
RATE

77. QUESTION
• Calculate the heart rate

78. THE QRS
AXIS
The QRS axis represents overall direction of the
heart’s electrical activity.
Abnormalities hint at:
Ventricular enlargement
Conduction blocks (i.e. hemiblocks)

79. THE QRS
AXIS
Normal QRS axis from -30° to
+90°.
-30° to -90° is referred to as a
left axis deviation (LAD)
+90° to +180° is referred to as
a right axis deviation (RAD)

80. DETERMINING
THE AXIS
The Quadrant Approach
The Equiphasic Approach

81. DETERMINING
THE AXIS
Predominantly
Positive
Predominantly
Negative
Equiphasic

82. THE QUADRANT
APPROACH
1. QRS complex in leads I and aVF
2. determine if they are predominantly positive or negative.
3. The combination should place the axis into one of the 4
quadrants below.

83. THE QUADRANT
APPROACH•
•
•
When LAD is present,
If the QRS in II is positive, the LAD is non-pathologic or the
axis is normal
If negative, it is pathologic.

84. QUADRANT APPROACH:
EXAMPLE 1
Negative in I, positive in aVF  RAD

85. QUADRANT APPROACH:
EXAMPLE 2
Positive in I, negative in aVF  Predominantly positive in II 
Normal Axis (non-pathologic LAD)

86. THE EQUIPHASIC
APPROACH
1. Most equiphasic QRS complex.
2. Identified Lead lies 90° away from the lead
3. QRS in this second lead is positive or Negative

87. QRS Axis = -30 degrees

88. QRS Axis = +90 degrees-KH

90. EQUIPHASIC
APPROACH
Equiphasic in aVF  Predominantly positive in I  QRS axis ≈ 0°

91. ARRHYTHMIA
FORMATION
Arrhythmias can arise from problems in the:
• Sinus node
• Atrial cells
• AV junction
• Ventricular cells

92. SA NODE PROBLEMS
The SANodecan:
• fire too slow
• fire too fast
SinusBradycardia
Sinus Tachycardia
Sinus Tachycardia may be an appropriate
response to stress.

93. ATRIAL CELL PROBLEMS
Atrial cells can:
• fire occasionally
from a focus
• fire continuously
due to a looping re-
entrant circuit
PrematureAtrial Contractions
(PACs)
Atrial Flutter

94. AVJUNCTIONAL
PROBLEMS
• The AVjunction can:
• fire continuously due
to a looping re-
entrant circuit
• block impulses
coming from the SA
Node
Paroxysmal
Supraventricular
Tachycardia
AV JunctionalBlocks

95. VENTRICULAR
CONDUCTION
Normal
Signal moves rapidly
through the ventricles
Abnormal
Signal moves slowly
through the ventricles

96. BRADYARRYTHMIA
• Classification

97. IMPULSE CONDUCTION & THE
ECG
Sinoatrial node
AVnode
Bundle of His
Bundle Branches

98. SINUS BRADYCARDIA

99. JUNCTIONAL RHYTHM

100. SA BLOCK
• Sinus impulses is blocked within the SA junction
• Between SAnode and surroundingmyocardium
• Abscent of complete Cardiac cycle
• Occures irregularly and unpredictably
• Present :Young athletes, Digitalis, Hypokalemia, Sick
Sinus Syndrome

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

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

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

104. PREMATURE ATRIAL
CONTRACTIONS
• Deviation from NSR
– These ectopic beats originate in the atria
(but not in the SAnode), therefore the
contour of the P wave, the PR interval,
and the timing are different than a
normally generated pulse from the SA
node.

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

106. SUPRAVENTRICULAR
ARRHYTHMIAS
• Atrial Fibrillation
• Atrial Flutter
• ParoxysmalSupraventricularTachycardia

107. RHYTHM #5
100 bpm
irregularly irregular
none
none
0.06 s
• Rate?
• Regularity?
• P waves?
• PR interval?
• QRS duration?
Interpretation? Atrial Fibrillation

108. ATRIAL FIBRILLATION
• Deviation from NSR
– No organized atrial depolarization, so no
normal P waves (impulses are not originating
from the sinus node).
– Atrial activity is chaotic (resulting in an
irregularly irregular rate).
– Common, affects 2-4%, up to 5-10% if > 80
years old

109. RHYTHM #6
70 bpm
regular
flutter waves
none
0.06 s
• Rate?
• Regularity?
• P waves?
• PR interval?
• QRS duration?
Interpretation? Atrial Flutter

110. RHYTHM #7
74 148 bpm
Regular  regular
Normal  none
0.16 s  none
0.08 s
• Rate?
• Regularity?
• P waves?
• PR interval?
• QRS duration?
Interpretation? Paroxysmal Supraventricular
Tachycardia (PSVT)

111. PSVT
• Deviation from NSR
– The heart rate suddenly speeds up, often
triggered by a PAC (not seen here) and the P
waves are lost.

112. VENTRICULAR
ARRHYTHMIAS
• Ventricular Tachycardia
• Ventricular Fibrillation

113. RHYTHM #8
160 bpm
regular
none
none
wide (> 0.12 sec)
• Rate?
• Regularity?
• P waves?
• PR interval?
• QRS duration?
Interpretation? Ventricular Tachycardia

114. VENTRICULAR
TACHYCARDIA
• Deviation from NSR
– Impulse is originating in the ventricles (no P
waves, wide QRS).

115. RHYTHM #9
• none
• irregularly
irreg. none
• none
• wide, if recognizable
• Rate?
• Regularity?
• P waves?
• PR interval?
• QRS duration?
Interpretation? Ventricular Fibrillation

116. VENTRICULAR
FIBRILLATION
• Deviation from NSR
– Completely abnormal.

117. AV NODAL BLOCKS
• 1stDegreeAV Block
• 2ndDegreeAV Block,TypeI
• 2ndDegreeAV Block,TypeII
• 3rdDegreeAV Block

118. RHYTHM #10
60 bpm
regular
normal
0.36 s
0.08 s
• Rate?
• Regularity?
• P waves?
• PR interval?
• QRS duration?
Interpretation? 1st Degree AV Block

119. 1ST DEGREE AV BLOCK
• Etiology: Prolonged conduction delay in the AV
node or Bundle of His.

120. FIRST DEGREE AV
BLOCK
• Delay in the conduction through the conducting system
• Prolong P-R interval
• All P waves are followed by QRS
• Associated with :ACRheumati Carditis, Digitalis, Beta
Blocker, excessive vagal tone, ischemia, intrinsic disease in
the AVjunction or bundle branchsystem.

121. SECOND DEGREE AV
BLOCK
• Intermittent failure of AV conduction
• Impulse blocked byAV node
• Types:
• Mobitz type 1 (Wenckebach Phenomenon)
• Mobitz type 2

122. RHYTHM #11
50 bpm
regularly irregular
nl, but 4th no QRS
lengthens
0.08 s
• Rate?
• Regularity?
• P waves?
• PR interval?
• QRS duration?
Interpretation? 2nd Degree AV Block, Type I

123. The 3 rules of "classic AV Wenckebach"
1. Decreasing RR intervals until pause;
2. Pause is less than preceding 2 RR intervals
3. RR interval after the pause is greater than RR prior to
pause.
MOBITZ TYPE 1 (WENCKEBACH
PHENOMENON)

124. MOBITZ TYPE 1 (WENCKEBACH
PHENOMENON)

125. RHYTHM #12
40 bpm
regular
nl, 2 of 3 no QRS
0.14 s
0.08 s
• Rate?
• Regularity?
• P waves?
• PR interval?
• QRS duration?
Interpretation? 2nd Degree AV Block, Type II

126. 2ND DEGREE AV
BLOCK, TYPE II
• Deviation from NSR
– Occasional P waves are completely blocked
(P wave not followed by QRS).

127. •Mobitz type 2
•Usually a sign of bilateral bundle branch disease.
•One of the branches should be completely blocked;
•most likely blocked in the right bundle
•P waves may blocked somewhere in the AV junction, the
His bundle.

128. RHYTHM #13
40 bpm
regular
no relation to QRS
none
wide (> 0.12 s)
• Rate?
• Regularity?
• P waves?
• PR interval?
• QRS duration?
Interpretation? 3rd Degree AV Block

129. 3RD DEGREE AV BLOCK
• Deviation from NSR
– The P waves are completely blocked in the
AVjunction; QRS complexes originate
independently from below the junction.

130. THIRD DEGREE HEART BLOCK
•CHB evidenced by the AV dissociation
•A junctional escape rhythm at 45 bpm.
•The PP intervals vary because of ventriculophasic sinus arrhythmia;

131. THIRD DEGREE HEART BLOCK
3rd degree AV block with a left ventricular escape rhythm,
'B' the right ventricular pacemaker rhythm is shown.

132. The nonconducted PAC's set up a long pause which
is terminated by ventricular escapes;
Wider QRS morphology of the escape beats
indicating their ventricular origin.
AV DISSOCIATION

133. AV DISSOCIATION
Due to Accelerated ventricular rhythm

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

135. ARRANGEMENT OF LEADS
ON THE EKG

136. ANATOMIC
GROUP(SEPTUM)

137. ANATOMIC GROUPS
(ANTERIOR WALL)

138. ANATOMIC GROUPS
(INFERIOR WALL)

139. ANATOMIC GROUPS
(LATERAL WALL)

140. ANATOMIC GROUPS
(SUMMARY)

141. VIEWS OF
THE HEART
Some leads get a
good view of the:
Lateral portion
of the heart
Anterior portion
of the heart
Inferior portion
of the heart

143. ST ELEVATION
One wayto
diagnose an
acute MI is to
look for
elevation of the
ST segment.

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

145. Anterior View of the Heart
The anterior portion of the heart is best viewed
using leads V1- V4.

146. ANTERIOR MYOCARDIAL
INFARCTION
If you see changes in leads V1- V4that
are consistent with a myocardial
infarction, you can conclude that it is an
anterior wall myocardial infarction.

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

148. Interpretation
Yes, this person is having an acute anterior
wallmyocardial infarction.

149. OTHER MI
LOCATIONS
Now that you know where to look for an
anterior wallmyocardial infarction let’s look at
how you would determine if the MI involves
the lateral wall or the inferior wallof the heart.

150. OTHER MI
LOCATIONS
First, take a look
again at this picture
of the heart.
Lateral portion
of the heart
Anterior portion
of the heart
Inferior portion
of the heart

151. OTHER MI
LOCATIONS
Second, 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

152. OTHER MI
LOCATIONS
Now, using these 3 diagrams let’s figure where to
look for a lateral wall and inferior wall MI.
Limb Leads Augmented Leads Precordial Leads

153. ANTERIOR MI
Remember the anterior portion of the heart is best
viewed using leads V1- V4.
Limb Leads Augmented Leads Precordial Leads

154. LATERAL MI
So what leads do you think
the lateral portion of the
heart is best viewed?
Limb Leads Augmented Leads Precordial Leads
Leads I, aVL, and V5- V6

155. INFERIOR MI
Now how about the
inferior portion of the
heart?
Limb Leads Augmented Leads Precordial Leads
Leads II, III and aVF

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

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

158. Putting it all Together
How about now?

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

160. POSTERIOR MI
• Posterior infarction accompanies 15-20% of STEMIs, usually
occurring in the context of an inferior or lateral infarction.
• Isolated posterior MI is less common (3-11% of infarcts).
• Posterior extension of an inferior or lateral infarct implies a
much larger area of myocardial damage, with an increased
risk of left ventricular dysfunction and death.
• Isolated posterior infarction is an indication for emergent
coronary reperfusion. However, the lack of obvious ST
elevation in this condition means that the diagnosis is often
missed.

161. HOW TO SPOT POSTERIOR
INFARCTION
• As the posterior myocardium is not directly visualised by the standard 12-
lead ECG, reciprocal changes of STEMI are sought in the anteroseptal leads
V1-3.
• Following changes in V1-3
• Horizontal ST depression
• Tall, broad R waves (>30ms)
• Upright T waves
• Dominant R wave (R/S ratio > 1) in V2

162. • The anteroseptal leads are directed from the anterior precordium
towards the internal surface of the posterior myocardium. Because
posterior electrical activity is recorded from the anterior side of the
heart, the typical injury pattern of ST elevation and Q waves
becomes inverted:
• ST elevation becomes ST depression
• Q waves become R waves
• Terminal T-wave inversion becomes an upright T wave

163. POSTERIOR LEADS
•V7 – Left posterior axillary line, in the same horizontal plane as V6.
•V8 – Tip of the left scapula, in the same horizontal plane as V6.
•V9 – Left paraspinal region, in the same horizontal plane as V6.

164. POSTERIOR INFARCTION IS
CONFIRMED BY THE PRESENCE
OF ST ELEVATION AND Q WAVES
IN THE POSTERIOR LEADS (V7-9).

165. INFEROLATERAL STEMI. POSTERIOR EXTENSION IS
SUGGESTED BY:
HORIZONTAL ST DEPRESSION IN V1-3
TALL, BROAD R WAVES (> 30MS) IN V2-3
DOMINANT R WAVE (R/S RATIO > 1) IN V2
UPRIGHT T WAVES IN V2-3

166. THE SAME PATIENT, WITH POSTERIOR LEADS
RECORDED. MARKED ST ELEVATION IN V7-9 WITH Q-
WAVE FORMATION CONFIRMS INVOLVEMENT OF THE
POSTERIOR WALL, MAKING THIS AN INFERIOR-LATERAL-
POSTERIOR STEMI (= BIG TERRITORY INFARCT!)

167. RIGHT VENTRICULAR MI
• Right ventricular infarction complicates up to 40% of inferior
STEMIs.
• Isolated RV infarction is extremely uncommon.
• Patients with RV infarction are very preload sensitive (due to
poor RV contractility) and can develop severe hypotension in
response to nitrates or other preload-reducing agents.
• Hypotension in right ventricular infarction is treated
with fluid loading, and nitrates are contraindicated.

168. HOW TO SPOT RIGHT
VENTRICULAR INFARCTION
• In patients presenting with inferior STEMI, right ventricular
infarction is suggested by the presence of:
• ST elevation in V1 – the only standard ECG lead that looks
directly at the right ventricle.
• ST elevation in lead III > lead II – because lead III is more
“rightward facing” than lead II and hence more sensitive to the
injury current produced by the right ventricle.
• Other useful tips for spotting right ventricular MI:
• ST elevation in V1 > V2.
• ST elevation in V1 + ST depression in V2 (= highly specific for RV
MI).
• Isoelectric ST segment in V1 with marked ST depression in V2.

169. RIGHT-SIDED LEADS
• The most useful lead is V4R,
which is obtained by placing the
V4 electrode in the 5th right
intercostal space in the
midclavicular line.
• ST elevation in V4R has a
sensitivity of 88%, specificity of
78% and diagnostic accuracy of
83% in the diagnosis of RV MI.

170. INFERIOR STEMI. RIGHT VENTRICULAR INFARCTION IS
SUGGESTED BY:
ST ELEVATION IN V1
ST ELEVATION IN LEAD III > LEAD II

171. IN SAME PATIENT THERE IS ST ELEVATION IN
V4R CONSISTENT WITH RV INFARCTION

172. SPECIFIC T WAVE
MORPHOLOGIES

174. LBBB V/S MI

175. SGARBOSSA CRITERIA
• In patients with left bundle branch block (LBBB)
or ventricular paced rhythm, infarct diagnosis based on the
ECG is difficult.
• The original three criteria used to diagnose infarction in
patients with LBBB are:
Concordant ST elevation > 1mm in leads with a positive QRS
complex (score 5)
Concordant ST depression > 1 mm in V1-V3 (score 3)
Excessively discordant ST elevation > 5 mm in leads with a -
ve QRS complex (score 2).

176. THESE CRITERIA ARE SPECIFIC, BUT NOT SENSITIVE FOR
MYOCARDIAL INFARCTION. A TOTAL SCORE OF ≥ 3 IS REPORTED
TO HAVE A SPECIFICITY OF 90% FOR DIAGNOSING MYOCARDIAL
INFARCTION.

178. • Benign early repolarization is an ECG pattern
most commonly seen in young, healthy patients < 50 years of
age.
• It produces widespread ST segment elevation that may mimic
pericarditis or acute MI.
• Up to 10-15% of ED patients presenting with chest pain will
have BER on their ECG, making it a common diagnostic
challenge for clinicians.
• The physiological basis of BER is poorly understood. However,
it is generally thought to be a normal variant that is not
indicative of underlying cardiac disease.
• BER is less common in the over 50s, in whom ST elevation is
more likely to represent myocardial ischaemia.
• It is rare in the over 70s.

179. HOW TO RECOGNISE BER
• Widespread concave ST elevation, most prominent in the mid-
to left precordial leads (V2-5).
• Notching or slurring at the J-point.
• Prominent, slightly asymmetrical T-waves that are concordant
with the QRS complexes (pointing in the same direction).
• The degree of ST elevation is modest in comparison to the T-
wave amplitude (less than 25% of the T wave height in V6)
• ST elevation is usually < 2mm in the precordial leads and <
0.5mm in the limb leads, although precordial STE may be up
to 5mm in some instances.
• No reciprocal ST depression to suggest STEMI (except in
aVR).
• ST changes are relatively stable over time (no progression on
serial ECG tracings)

180. TYPICAL MORPHOLOGY OF BER

181. THE DIFFERENTIAL FEATURES
BETWEEN BER AND PERICARDITIS
Features suggesting
BER
• ST elevation limited to the
precordial leads
• Absence of PR depression
• Prominent T waves
• ST segment / T wave ratio <
0.25
• Characteristic “fish-hook”
appearance in V4
• ECG changes usually stable
over time (i.e non-progressive)
Features suggesting
pericarditis
• Generalised ST elevation
• Presence of PR depression
• Normal T wave amplitude
• ST segment / T wave ratio >
0.25
• Absence of “fish hook”
appearance in V4
• ECG changes evolve slowly
over time

183. • The de Winter ECG pattern is an anterior STEMI
equivalent that presents without obvious ST segment
elevation. First reported by first reported de Winter in 2008
• Key diagnostic features include ST depression and peaked T
waves in the precordial leads.
• The de Winter pattern is seen in ~2% of acute LAD
occlusions andis under-recognised by clinicians.
• Unfamiliarity with this high-risk ECG pattern may lead to
under-treatment (e.g. failure of cath lab activation), with
attendant negative effects on morbidity and mortality.

185. • Wellens syndrome is a pattern of deeply inverted or biphasic T
waves in V2-3, which is highly specific for a critical stenosis of
the left anterior descending artery (LAD).
• Patients may be pain free by the time the ECG is taken and
have normally or minimally elevated cardiac enzymes;
however, they are at extremely high risk for extensive anterior
wall MI within the next few days to weeks.
• Due to the critical LAD stenosis, these patients usually
require invasive therapy; do poorly with medical management;
and may suffer MI or cardiac arrest if inappropriately stress
tested.

187. BRUGADA SYNDROME
• Brugada Syndrome is an ECG abnormality with a high incidence of
sudden death in patients with structurally normal hearts.
• It is due to a mutation in the cardiac sodium channel gene (sodium
channelopathy).
• ECG changes can be transient with Brugada syndrome and can also
be unmasked or augmented by multiple factors:
• Fever
• Ischaemia

188. • Multiple Drugs
• Sodium channel blockers eg: Flecainide, Propafenone
• Calcium channel blockers
• Alpha agonists
• Beta Blockers
• Nitrates
• Cholinergic stimulation
• Cocaine
• Alcohol
• Hypokalaemia
• Hypothermia
• Post DC cardioversion

189. • Coved ST segment elevation
>2mm in >1 of V1-V3 followed
by a negative T wave.
• This is the only ECG
abnormality that
is potentially diagnostic.
• It is often referred to
as Brugada sign.
Clinical criteria
• Documented ventricular
fibrillation (VF) or
polymorphic ventricular
tachycardia (VT).
• Family history of sudden
cardiac death at <45 years old
.
• Coved-type ECGs in family
members.
• Inducibility of VT with
programmed electrical
stimulation .
• Syncope.
• Nocturnal agonal respiration.
Diagnostic Criteria

190. BUNDLE BRANCH
BLOCKS

191. NORMAL IMPULSE CONDUCTION
Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers

192. BUNDLE BRANCH BLOCKS
So, conduction in the
Bundle Branches and
Purkinje fibers are seen
as the QRS complex on
the ECG.
Therefore, a conduction
block of the Bundle
Branches would be
reflected as a change in
the QRS complex.
Right
BBB

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

194. RIGHT BUNDLE BRANCH
BLOCKS
What QRS morphology is characteristic?
For RBBB the wide QRS complex assumes a
unique, virtually diagnostic shape in those
leads overlying the right ventricle (V1 and V2).
V1
“Rabbit Ears”

195. RBBB

197. LEFT BUNDLE BRANCH
BLOCKS
What QRS morphology is characteristic?
For LBBB the wide QRS complex assumes a
characteristic change in shape in those leads
opposite the left ventricle (right ventricular
leads - V1 and V2).
Broad,
deep S
waves
Normal

201. FASCICULAR BLOCKS

202. LEFT ANTERIOR FASCICULAR
BLOCK/ LEFT ANTERIOR
HEMIBLOCK

203. • ECG Criteria for Left Anterior Fascicular Block (LAFB)
• Left axis deviation (usually between -45 and -90 degrees)
• Small Q waves with tall R waves (= ‘qR complexes’) in leads I
and aVL
• Small R waves with deep S waves (= ‘rS complexes’) in leads
II, III, aVF
• QRS duration normal or slightly prolonged (80-110 ms)
• Prolonged R wave peak time in aVL > 45 ms
• Increased QRS voltage in the limb leads

204. RIGHT ANTERIOR FASCICULAR
BLOCK/ RIGHT ANTERIOR
HEMIBLOCK

205. • ECG Criteria for Left Posterior Fascicular Block (LPFB)
• Right axis deviation (RAD) (> +90 degrees)
• Small R waves with deep S waves (= ‘rS complexes‘) in leads I
and aVL
• Small Q waves with tall R waves (= ‘qR complexes‘) in leads II,
III and aVF
• QRS duration normal or slightly prolonged (80-110ms)
• Prolonged R wave peak time in aVF
• Increased QRS voltage in the limb leads
• No evidence of right ventricular hypertrophy
• No evidence of any other cause for right axis deviation

206. BIFASCICULAR BLOCK

207. • Bifascicular block is the combination of RBBB with
either LAFB or LPFB.
• Conduction to the ventricles is via the single remaining
fascicle.
• The ECG will show typical features of RBBB plus either left or
right axis deviation.
• RBBB + LAFB is the most common of the two patterns.
• Bifascicular block is a sign of extensive conducting system
disease, although the risk of progressing to complete heart
block is thought to be relatively low (1% per year in one cohort
study of 554 patients).
• NB. Some authors also consider LBBB to be a ‘bifascicular
block’, because both fascicles of the left bundle branch are
blocked

208. TRIFASCICULAR BLOCK
• Trifascicular block (TFB) refers to the presence of
conducting disease in all three fascicles:
• Right bundle branch (RBB)
• Left anterior fascicle (LAF)
• Left posterior fascicle (LPF)

209. • Incomplete vs complete TFB
• Trifascicular block can be incomplete or complete, depending
on whether all three fascicles have completely failed or not.
• Incomplete trifascicular block
• Incomplete (“impending“) trifascicular block can be inferred
from one of two electrocardiographic patterns:
• Fixed block of two fascicles (i.e. bifascicular block) with
delayed conduction in the remaining fascicle
(i.e. 1st or 2nd degree AV block).
• Fixed block of one fascicle (i.e. RBBB) with intermittent
failure of the other two fascicles (i.e.
alternating LAFB / LPFB).

210. • Complete trifascicular block
• Complete trifascicular block produces 3rd degree AV
block with features of bifascicular block.
• This is because the escape rhythm usually arises from the
region of either the left anterior or left posterior fascicle (distal
to the site of block), producing QRS complexes with the
appearance of RBBBplus either LPFB or LAFB respectively.

211. • Patterns of TFB
• The most common pattern referred to as “trifascicular block”
is the combination of bifascicular block with 1st degree AV
block.
• Incomplete trifascicular block
• Bifascicular block + 1st degree AV block (most common)
• Bifascicular block + 2nd degree AV block
• RBBB + alternating LAFB / LPFB
• Complete trifascicular block
• Bifascicular block + 3rd degree AV block

212. EXAMPLE 1
INCOMPLETE TRIFASCICULAR BLOCK:
RIGHT BUNDLE BRANCH BLOCK
+LEFT AXIS DEVIATION (= LEFT ANTERIOR FASCICULAR
BLOCK)
+FIRST DEGREE AV BLOCK

213. EXAMPLE 2
COMPLETE TRIFASCICULAR BLOCK:
RIGHT BUNDLE BRANCH BLOCK
+LEFT AXIS DEVIATION (= LEFT ANTERIOR FASCICULAR
BLOCK)
+THIRD DEGREE AV BLOCK

214. ELECTROLYTE
IMBALANCES

215. HYPERKALEMIA

217. SEVERE HYPERKALEMIA

218. HYPOKALEMIA

219. HYPOKALEMIA

220. HYPOKALEMIA

221. HYPERCALCEMIA

222. HYPOCALCEMIA

225. ACUTE PERICARDITIS

226. ACUTE PERICARDITIS

227. CARDIAC TAMPONADE

228. PERICARDIAL EFFUSION-
ELECTRICAL ALTERANS

229. HYPOTHERMIA-OSBORNE WAVE

230. HYPOTHERMIA-
GIANT OSBORNE WAVES