ECG from A TO Z

3. 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.

6. mcl
mal

8. V1
V1
V2
V2
V3
V3
V4
V4
V5
V5
Horizontal plane - the six chest leads
V6
V6
RA
LA
LV
RV
6.5

9. 9
The 12-Leads
The 12-leads include:
–3 Limb leads
(I, II, III)
–3 Augmented leads
(aVR, aVL, aVF)
1942- Goldberger increased Wilson’s Unipolar
lead voltage by 50%
–6 Precordial leads
(V1- V6)
1938 -AHA and Cardiac society of great Britain
1906 - William Einthoven diagnoses some heart
problems , 1924 - the noble prize

10. 60 – 100 times a minute
40 – 60 times a minute
20 – 40 times a minute

11. 1111
Cardiac Conduction

12. Impulse Conduction & the ECG
Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers
The “PQRST”

14. Normal Components of the EKG Waveform

16. ECG RULES
• Professor Chamberlains 10 rules of normal:-
1. PR interval should be 120 to 200 milliseconds or 3 to 5 little squares
2. The width of the QRS complex should not exceed 110 ms, less than 3
little squares
3. The QRS complex should be dominantly upright in leads I and II
4. QRS and T waves tend to have the same general direction in the limb
leads
5. All waves are negative in lead aVR
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
7. The ST segment should start isoelectric
8. The P waves should be upright in I, II, and V2 to V6
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
10. The T wave must be upright in I, II, V2 to V6

17. R1
R2R3
R4
R5
R6
R7
R8
R9NO ABNORMAL Q
R10

19. STANDARDISATION ECG
amplitude scale
Normal amplitude
10 mm/mV
Half amplitude
5 mm/mV
Double amplitude
20 mm/mV

21. Why “1500 / X”?
• Paper Speed: 25 mm/ sec
• 60 seconds / minute
• 60 X 25 = 1500 mm / minute
• 60 X 5 = 300 big square / minute
• Take 6 sec strip (30 large boxes)
• Count the P/R waves X 10
OR

22. DR/ SHAFEI LASHEEN
Step 1: Calculate Rate when
rhythm is regular
– Find a R wave that lands on a bold line.
– Count the # of large boxes to the next R wave.
– HR = 300/ no large boxes between R-R interval
– Count the # of small boxes to the next R wave
– HR= 1500/ no small boxes between R-R interval
R wave

23. DR/SHAFEI LASHEEN
HR if irregular rhythm
– Count the # of R waves in a 6 second rhythm
strip, then multiply by 10.
– Reminder: all rhythm strips in the Modules are
6 seconds in length.
Interpretation?
9 x 10 = 90 bpm
3 sec 3 sec

24. DR/ SHAFEI LASHEEN
Step 2: Determine rhythm
• 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
R R

25. Regularity of Rhythm

31. DR/ SHAFEI LASHEEN
Axis

34. True LAD
• So again, if lead I is positive and aVF is
negative, we suspect LAD
• To diagnose true LAD, we examine lead II:
– If lead II is positive, axis = 0° to –30°
– If lead II is negative , axis = –30° to –90°

35. Extreme RAD
• If lead I is negative AND aVF is also
negative – extreme RAD
• Clue: If aVR is positive = extreme RAD
• This is seen with rare situations such as VT or
Pacemakers
• In general we should never have an axis over
here!

37. DR/ SHAFEI LASHEEN
Right axis deviation

40. P-wave
Normal values
1. up in all leads except
AVR.
2. Duration.
< 2.5 mm.
3. Amplitude.
< 2.5 mm.
Extreme RT. axis
Abnormalities
1. Inverted P-wave
• Junctional rhythm.
2. Wide P-wave (P- mitrale)
• LAE
3. Peaked P-wave (P-pulmonale)
• RAE
4. Saw-tooth appearance
• Atrial flutter
5. Absent normal P wave
• Atrial fibrillation

41. P Pulmonale
P Mitrale

42. Slide 9

43. Slide 15

44. DR/ SHAFEI LASHEEN
Step 3: Assess the P waves
• Are there P waves?
• Do the P waves all look alike?
• Do the P waves occur at a regular rate?
• Is there one P wave before each QRS?
Interpretation? Normal P waves with 1 P
wave for every QRS

46. PR Interval
Measured from the beginning of the P wave to the
beginning of the Q wave.
Normal PR interval ranges from 0.12 to 0.20 second.
PR interval

47. PR interval
Definition: the time
interval between
beginning of P-wave
to beginning of QRS
complex.
Normal PR interval
3-5mm or 3-5 small
squares on ECG
graph (0.12-0.2 sec)
Abnormalities
1. Short PR interval
• WPW syndrome
2. Long PR interval
• First degree heart
block

48. Slide 17

49. Slide 44

50. DR/ SHAFEI LASHEEN
Step 4: Determine PR interval
• Normal: 0.12 - 0.20 seconds.
(3 - 5 boxes)
Interpretation? 0.12 seconds

52. QRS Complex
Represents complete
ventricular
depolarization
QRS complex
QRS Complex Variants
QRS Complex

53. QRS complex
Normal values
• Duration: < 2.5 mm.
• Morphology:
progression from Short
R and deep S (r/s) in V1
to tall R and short S in
V6 with small Q in V5-6.
Abnormalities:
1. Wide QRS complex
• Bundle branch block.
• Ventricular rhythm.
2. Tall R in V1
• RVH.
• RBBB.
• Posterior MI.
• WPW syndrome.
3. abnormal Q wave
[ > 25% of R wave]
• MI.
• Hypertrophic
cardiomyopathy.
• Normal variant.

54. Small voltage QRS
• Defined as < 5 mm peak-to-peak in all
limb leads or <10 mm in precordial chest
leads.
• causes — pulmonary disease,
hypothyroidism, obesity,
cardiomyopathy.
• Acute causes — pleural and/or
pericardial effusions

56. DR/ SHAFEI LASHEEN
Step 5: QRS duration
• Normal: 0.04 - 0.12 seconds.
(1 - 3 boxes)
Interpretation? 0.08 seconds

58. Q Wave
Represents the
beginning of septal
depolarization
The first negative
deflection off of the
baseline
Q Wave

59. Q WAVES
• Q waves <0.04 second.
• That’s is less than one small square
duration.
• Height <25% or < 1/4 of R wave height.

60. Normal Q wave

61. 61
61
Normal Q waves
Notice the small
Normal Q in Lead I

62. Abnormal Q waves
• The duration or width of Q waves
becomes more than one small square on
ECG graph.
• The depth of Q wave becomes more than
25% of R wave.
• The above changes comprise pathological
Q wave and happens commonly in
myocardial infarction and septal
hypertrophy.

63. Q wave in MI

64. 64
64
Pathological Q wave
Notice the deep & wide
Infarction Q in Lead I

65. Q wave in septal hypertrophy

67. R Wave
Indicates left
ventricular
depolarization
The first positive
deflection off the
baseline
R Wave

68. Normal upward progression of R
wave from V1 to V6
V1
V2
V3
V4
V5
V6
The R wave in the precordial leads must grow from V1 to at least V4

71. T-wave
Normal values.
1.amplitude:
< 10mm in the chest leads.
Abnormalities:
1. Peaked T-wave:
• Hyper-acute MI.
• Hyperkalemia.
• Normal variant
.
2. T- inversion:
• Ischemia.
• Myocardial infarction.
• Myocarditis
• Ventricular strain
• BBB.
• Hypokalemia.
• Digoxin effect.

73. NORMAL ST- SEGMENT
it's isoelectric.
[i.e. at same level of PR
or PQ segment at least
in the beginning]

74. Abnormalities
1. ST elevation:
More than one small
square
• Acute MI.
• Prinzmetal angina.
• Acute pericarditis.
• Early repolarization
ST depression:
More than one small
square
• Ischemia.
• Ventricular strain.
• BBB.
• Hypokalemia.
• Digoxin effect.

75. Abnormalities of ST- segment

76. Slide 11

77. Slide 12

79. QT- interval
Definition: Time interval between beginning of
QRS complex to the end of T wave.
Normally: At normal HR: QT ≤ 11mm (0.44
sec)
Abnormalities:
1. Prolonged QT interval: hypocalcemia and
congenital long QT syndrome.
2. Short QT interval: hypercalcemia.

80. DR/ SHAFEI LASHEEN
QTc interval
@ HR 70 QT< 0.40 sec
@ HR 80 QT< 0.38 sec
@ HR 60 QT< 0.42 sec
< 0.44 s > 0.44 s
Normal Long QT
A prolonged QT can be very dangerous. It may predispose an individual to a type of
ventricular tachycardia called Torsades de Pointes. Causes include drugs, electrolyte
abnormalities, CNS disease, post-MI, and congenital heart disease.
Torsades de Pointes
Long QT

81. EKG Intervals
1. P-wave < 0.110 sec (approximately 3 small boxes)
2. PR interval = beginning of the P-wave to the
beginning of QRS. Normal = 0.120 – 0.200 sec
3. QRS interval = from the first deflection to return to
the baseline. Normal < 0.120 sec
4. QT interval = beginning of the QRS to the END of
the T-wave. Normal < 0.450 sec

83. U Wave
Represents the last phase of
repolarization.
The exact significance is
unknown.
Characteristic of
hypokalemia.
May predispose to
ventricular arrhythmias.
U Wave

84. DR/ SHAFEI LASHEEN
ECG Rhythm Interpretation
Normal Sinus Rhythm

85. 1. Every QRS is preceded by a P-wave
2. P-waves appear normal, that is they are of sinus
node origin:
A. Normal Morphology:
1. P-wave duration < 0.12 sec (< 3 boxes)
2. P-wave height < 2.5 mm
B. Normal Axis – upright P-waves in lead II
Sinus Rhythm…or Not!

86. DR/ SHAFEI LASHEEN
Rhythm Summary
• Rate 90-95 bpm
• Regularity regular
• P waves normal
• PR interval 0.12 s
• QRS duration 0.08 s
Interpretation? Normal Sinus Rhythm

87. DR/ SHAFEI LASHEEN
NSR Parameters
• Rate 60 - 100 bpm
• Regularity regular
• P waves normal
• PR interval 0.12 - 0.20 s
• QRS duration 0.04 - 0.12 s
Any deviation from above is sinus Tachycardia,
sinus bradycardia or an arrhythmia

88. DR .SHAFEI LASHEEN 2010

90. What types of pathology can we identify
and study from EKGs?

91. DR/ SHAFEI LASHEEN
Arrhythmia Formation
Arrhythmias can arise from problems in the:
• Sinus node
• Atrial cells
• AV junction
• Ventricular cells

92. DR/ SHAFEI LASHEEN
SA Node Problems
The SA Node can:
• fire too slow
• fire too fast
SAN diseases
Sinus Arrhythmia
Sinus Bradycardia
Sinus Tachycardia
(Sinus Tachycardia may be an appropriate
response to stress.)

93. DR / SHAFEI LASHEEN
Rhythm #1
30 bpm• Rate?
• Regularity? regular
normal
0.10 s
• P waves?
• PR interval? 0.12 s
• QRS duration?
Interpretation? Sinus Bradycardia

94. DR/ SHAFEI LASHEEN
Rhythm #2
130 bpm• Rate?
• Regularity? regular
normal
0.08 s
• P waves?
• PR interval? 0.16 s
• QRS duration?
Interpretation? Sinus Tachycardia

95. Sinus block

96. Missed cycle

97. Sick Sinus Syndrome
 Sinoatrial block (note the pause
is twice the P-P interval)
Sinus arrest with pause of 4.4 s
before generation and conduction
of a junctional escape beat
Severe sinus bradycardia

98. Sinus Arrhythmia
inspiration expiration

99. DR/ SHAFEI LASHEEN
Atrial Cell Problems
• fire occasionally
from a focus
• fire continuously due
to a looping re-
entrant circuit
Premature Atrial
Contractions (PACs)
Atrial Flutter

100. DR/ SHAFEI LASHEEN
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.

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

103. Atrial Fibrillation

104. Atrial Fibrillation
(A-fib)

105. DR/ SHAFEI LASHEEN
Rhythm #5
100 bpm• Rate?
• Regularity? irregularly irregular
none
0.06 s
• P waves?
• PR interval? none
• QRS duration?
Interpretation? Atrial Fibrillation

107. Atrial Flutter

108. DR/ SHAFEI LASHEEN
Rhythm #6
70 bpm• Rate?
• Regularity? regular
flutter waves
0.06 s
• P waves?
• PR interval? none
• QRS duration?
Interpretation? Atrial Flutter

109. DR/ SHAFEI LASHEEN
AV Junctional Problems
The AV junction can:
• fire continuously
due to a looping re-
entrant circuit
• block impulses
coming from the SA
Node
Paroxysmal
Supraventricular
Tachycardia
AV Junctional Blocks

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

111. AVNR tachycardia

112. Junctional Premature Beat
• single ectopic beat that originates in the AV node
or
• Bundle of His area of the condunction system
• – Retrograde P waves immediately preceding the
QRS
• – Retrograde P waves immediately following the
QRS
• – Absent P waves (buried in the QRS)

113. Premature Junctional
Complexes (PJC)

114. Junctional Escape Beat

115. Junctional Rhythm

116. DR/ SHAFEI LASHEEN
Ventricular Cell Problems
Ventricular cells can:
• fire occasionally
from 1 or more foci
• fire continuously
from multiple foci
• fire continuously
due to a looping re-
entrant circuit
Premature Ventricular
Contractions (PVCs)
Ventricular Fibrillation
Ventricular Tachycardia

117. DR/ SHAFEI LASHEEN
Ventricular Conduction
Normal
Signal moves rapidly
through the ventricles
Abnormal
Signal moves slowly
through the ventricles

118. Premature Ventricular
Complex (PVC)
*
*

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

120. DR/ SHAFEI LASHEEN
PVCs

125. Ventricular Tachycardia (VT)

126. DR/ SHAFEI LASHEEN
160 bpm• Rate?
• Regularity? regular
none
wide (> 0.12 sec)
• P waves?
• PR interval? none
• QRS duration?
Interpretation? Ventricular Tachycardia

127. Ventricular Fibrillation (VF)
*
* *
*
*
**
***

128. DR/ SHAFEI LASHEEN
Rhythm #9
none• Rate?
• Regularity? irregularly irreg.
none
wide, if recognizable
• P waves?
• PR interval? none
• QRS duration?
Interpretation? Ventricular Fibrillation

129. Torsade des points

133. AV Junctional Blocks

134. AV Blocks
AV Node Bundle of His
Right Bundle Branch Left Bundle Branch
Anterior Fascicle of Posterior Fascicle of
Left Bundle Left Bundle

135. DR/ SHAFEI LASHEEN

136. Classification of AV Heart Blocks
Degree AV Conduction Pattern
1St Degree Block Uniformly prolonged PR
interval
2nd Degree, Mobitz Type I
Progressive PR interval
prolongation
2nd Degree, Mobitz Type II Sudden conduction failure
3rd Degree Block No AV conduction

137. DR/ SHAFEI LASHEEN
60 bpm• Rate?
• Regularity? regular
normal
0.08 s
• P waves?
• PR interval? 0.36 s
• QRS duration?
Interpretation? 1st Degree AV Block

138. Second Degree AV Block
• Mobitz type I or Winckebach
• Mobitz type II

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

140. DR/ SHAFEI LASHEEN
40 bpm• Rate?
• Regularity? regular
nl, 2 of 3 no QRS
0.08 s
• P waves?
• PR interval? 0.14 s
• QRS duration?
Interpretation? 2nd Degree AV Block, Type II

141. Third Degree AV Block
(Complete Heart Block)
SA Node conducts at its AV Node conducts at its
inherent rate of 60-100 BPM inherent rate of 40-60
BPM
Two independent pacemakers

142. Third Degree AV Block
(Complete Heart Block)
P P P P P P P P P
QRS QRS QRS
Atria
AV Node
Ventricles
BLOCK

144. DR/ SHAFEI LASHEEN
40 bpm• Rate?
• Regularity? regular
no relation to QRS
wide (> 0.12 s)
• P waves?
• PR interval? none
• QRS duration?
Interpretation? 3rd Degree AV Block

145. Acute Coronary Syndrome

146. ECG assessment
ST Elevation or new LBBB
STEMI
Non-specific ECG
Unstable Angina
ST Depression or dynamic
T wave inversions
NSTEMI

148. DR/ SHAFEI LASHEEN
ECG Rhythm Interpretation
Acute Myocardial Infarction

149. DR/ SHAFEI LASHEEN
ST Elevation and
non-ST Elevation MIs

150. DR/ SHAFEI LASHEEN
ECG Changes & the Evolving MI
There are two
distinct patterns of
ECG change
depending if the
infarction is:
–ST Elevation (Transmural or Q-wave), or
–Non-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation

151. DR/ SHAFEI LASHEE
ECG Changes
Ways the ECG can change include:
Appearance
of pathologic
Q-waves
T-waves
peaked flattened inverted
ST elevation &
depression

153. DR/ SHAFEI LASHEEN

154. Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
Q
TST
R
P
Q
ST
P
Q
T
ST
R
P
S
T
P
Q
T
ST
R
P
Q
T

155. DR/ SHAFEI LASHEEN
Views of the Heart
Some leads get a
good view of the:
Anterior portion
of the heart
Lateral portion
of the heart
Inferior portion
of the heart

158. Anatomic Groups
(Septum)

159. Anatomic Groups
(Anterior Wall)

160. Anatomic Groups
(Lateral Wall)

161. Anatomic Groups
(Inferior Wall)

162. Anatomic Groups
(Summary)

164. Which part of the heart is affected ?
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
• Leads V1, V2, V3, and V4 =
Anterior Wall MI

165. Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left
coronary
Artery or LAD

166. Anterior Wall MI

167. AWMI (pardee’s sign)
The convex upwards ST elevation which is classical of acute myocardial infarction was
described by Pardee in 1920 and has been called the “Pardee’s sign”

168. DR/ SHAFEI LASHEEN
ST Elevation (cont)
Elevation of the ST
segment (greater
than 1 small box)
in 2 leads is
consistent with a
myocardial
infarction.

169. What part of the heart is affected ?
 I, aVL, V5 and V6
Lateral wall of left ventricle
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6

170. Lateral infarction
Lateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left
circumflex
coronary
artery

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

172. DR/ SHAFEI LASHEEN
Infarct: Is the ST elevation
or depression?
Yes! Elevation in V2-V6, I and avL.
Depression in II, III and avF.

174. What part of the heart is affected ?
II, III, aVF =
Inferior Wall
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6

175. Inferior infarction
Inferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right
coronary
artery

176. DR SHAFEI LASHEE
Inferior Wall MI
This is an inferior MI. Note the ST elevation in
leads II, III and aVF.

177. 177
177
Acute True Posterior MI

181. inferior/posterior STEMI with RV involvement

182. STEMI equivalent

183. Acute pericarditis

184. Acute pulmonary embolism

185. 45 yo female 1 week post-op with shortness of breath

186. Findings
• Accelerated junctional
rhythm
• Right axis deviation
• “S1Q3T3” pattern
• Clinical history and
EKG most consistent
with acute PE

188. DR/ SHAFEI LASHEEN
Non-ST Elevation Infarction
ST depression & T-wave inversion
The ECG changes seen with a non-ST elevation infarction are:
Before injury Normal ECG
ST depression & T-wave inversion
ST returns to baseline, but T-wave
inversion persists
Ischemia
Infarction
Fibrosis

189. ST Depression or Dynamic T wave
Inversions

190. DR/ SHAFEI LASHEEN
Non-ST Elevation Infarction
Here’s an ECG of an evolving non-ST elevation MI:
Note the ST
depression and
T-wave
inversion in
leads V2-V6.
Question:
What area of
the heart is
infarcting?
Anterolateral

192. Hypertrophy

193. DR/ SHAFEI LASHEEN
Hypertrophy
In this step of the 12-lead ECG analysis, we use the ECG to
determine if any of the 4 chambers of the heart are enlarged or
hypertrophied. We want to determine if there are any of the
following:
– Right atrial enlargement (RAE)
– Left atrial enlargement (LAE)
– Right ventricular hypertrophy (RVH)
– Left ventricular hypertrophy (LVH)

194. Slide 15

196. DR/ SHAFEI LASHEEN
– To diagnose RAE you can use the following criteria:
• II P > 2.5 mm, or
• V1 or V2 P > 1.5 mm
Right atrial enlargement

197. DR/ SHAFEI LASHEEN
Left atrial enlargement
– To diagnose LAE you can use the following criteria:
• II > 0.04 s (1 box) between notched peaks, or
• V1 Neg. deflection > 1 box wide x 1 box deep

199. 199
199
Ventricular Hypertrophy
• Ventricular Muscle
Hypertrophy
• QRS voltages in V1 and V6, L
1 and aVL
• We may have to record to ½
standardization
• T wave changes opposite to
QRS direction
• Associated Axis shifts
• Associated Atrial hypertrophy

200. DR/ SHAFEI LASHEEN
Left Ventricular
Hypertrophy

201. DR// SHAFEI LASHEEN
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS
complexes?
LVH ECHOcardiogram
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.

202. Criteria for LVH
• Sokolow-Lyon
– S v1+R v5/v6>35mm
– R I+S III>25mm
– R avl>11mm
• Cornell
– S v3+R avl >28 (men)
>20 (women)
• Romhilt-Estes
– LV strain 3
– LAE 3
– LAD 2
– QRS duration 1
– R v5/v6>3 3
– Sv1/v2>3 3
– Largest R or S>2 3
5 or more points suggests LVH

203. 203
203
Left Ventricular Hypertrophy

204. LV+LA

205. 205
205
Right Ventricular Hypertrophy

207. DR/ SHAFEI LASHEEN
Bundle Branch Blocks

208. DR / SHAFEI LASHEE
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).

209. 209
209
Complete RBBB

210. DR/SHAFEI LASHEEN
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).

211. 211
211
Complete LBBB

215. Miscellaneous

219. K Ca

221. Hyperkalaemia

222. K=9.4 mmol/l

223. Hypokalaemia

224. K= 1.5

225. Hypocalcaemia

226. Pericardial Effusion (electrical
alternans)

227. Hypothermia (osborne wave)

229. Arrythmogenic RV dysplasia
(Epsilon wave)

230. Digitalis toxicity

231. SAH(t wave +long QT)

232. WPW syndrome

233. WPW + AF

234. Ventricular Pacemaker
(Single Chamber)
pacemaker

236. Dual Paced Rhythm
pacemaker

237. AV pacing

238. Cable reversal

240. Dextrocardia

241. Artifacts in Parkinson’s pt.

242. Movements Artifacts

245. Electric noise

246. DR .SHAFEI LASHEEN 2010