ECG Presentation,Nice Interpretation

1. ECG BASICS
By
Dr Bashir Ahmed Dar
Chinkipora Sopore
Kashmir
Associate Professor
Medicine
Email
drbashir123@gmail.com

2. 





From Right to Left
Dr.Smitha associate
prof gynae
Dr Bashir associate
professor Medicine
Dr Udaman
neurologist
Dr Patnaik HOD
ortho
Dr Tin swe aye paeds

3. 





From RT to Lt
Professor Dr Datuk
rajagopal N
Dr Bashir associate
professor medicine
Dr Urala HOD
gynae
Dr Nagi reddy
tamma HODopthomology
Dr Setharamarao
Prof ortho

5. ELECTROGRAPHY MADE
EASY
 ULTIMATE
AIM TO HELP PATIENTS

6. ECG machine

7. Limb and chest leads
 When
an ECG is taken we put 4 limb leads
or electrodes with different colour codes on
upper and lower limbs one each at wrists
and ankles by applying some jelly for close
contact.
 We also put six chest leads at specific areas
over the chest
 So in reality we see only 10 chest leads.

8. Position of limb and chest leads

Four limb leads

Six chest leads
V1- 4th intercostal space to the right of sternum
V2- 4th intercostal space to the left of sternum
V3- halfway between V2 and V4
V4- 5th intercostal space in the left mid-clavicular line
V5- 5th intercostal space in the left anterior axillary line
V6- 5th intercostal space in the left mid axillary line







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

10. Colour codes given by AHA

11. ECG Paper: Dimensions
5 mm
1 mm
0.1 mV
0.04 sec
0.2 sec
Speed = rate
Voltage
~Mass

12. ECG paper and timing


ECG paper speed
Voltage calibration 1 mV
= 25mm/sec
= 1cm

ECG paper - standard calibrations
– each small square
= 1mm
– each large square
= 5mm

Timings
– 1 small square
– 1 large square
– 25 small squares
– 5 large squares
=
=
=
=
0.04sec
0.2sec
1sec
1sec

13.  After
applying these leads on different
positions then these leads are connected to a
connector and then to ECG machine.
 The speed of machine kept usually
25mm/second.calibration or standardization
done while machine is switched on.

14. ECG paper
1 Small square = 0.04 second
2 Large squares = 1 cm
1 Large square = 0.2 second
5 Large squares = 1 second
Time
6.1

15.  The
first step while reading ECG is to look
for standardization is properly done.
 Look for this mark and see that this mark
exactly covers two big squares on graph.

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

17. ECG WAVES
 You
will see then base line or isoelectric
line that is in line with P-Q interval and
beginning of S-T segment.
 From this line first positive deflection will
arise as P wave then other waves as shown
in next slide.
 Small negative deflections Q wave and S
wave also arise from this line.

18. ECG WAVES

19. The Normal ECG
Normal Intervals:
PR 0.12-0.20s
QRS duration <0.12s
QTc 0.33-0.43s

20. Simplified normal Position of
leads on ECG graph
 Lead
1# upward PQRS
 Lead 2# upward PQRS
 Lead 3# upward PQRS
 Lead AVR#downward or negative PQRS
 Lead AVL# upward PQRS
 Lead AVF# upwards PQRS

21. Simplified normal Position of
leads on ECG graph
 Chest
lead V1# negative or downward
PQRS
 Chest leads V2-V3-V4-V5-V6 all are
upright from base line .The R wave slowly
increasing in height from V1 to V6.
 So in normal ECG you see only AVR and
V1 as negative or downward defelections as
shown in next slide.

22. Normal ECG
Slide 13

23. NSR

24. P-wave
 Normal
P wave length from beginning of P
wave to end of P wave is 2 and a half small
square.
 Height of P wave from base line or
isoelectric line is also 2 and a half small
square.

25. P-wave
Normal values
1. up in all leads except
AVR.
2. Duration.
< 2.5 mm.
3. Amplitude.
< 2.5 mm.
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

26. P wave height 2 and half small
squares ,width also 2 and half
small square
Slide 9

27. Shape of P wave
 The
upward limb and downward limbs of P
wave are equal.
 Summit or apex of P wave is slightly
rounded.

28. P pulmonale & P mitrale
P
pulmonale-Summit or apex of P wave
becomes arrow like pointed or pyramid
shape,the height also becomes more than
two small squares from base line.
 P waves best seen in lead 2 and V1.

29. P pulmonale & P mitrale
P
mitrale- the apex or summit of p wave
may become notched .the notch should be at
least more than one small square.
 Duration of P becomes more than two and a
half small squares.

30. Slide 14

31. Slide 16

32. Left Atrial Enlargement
Criteria
P wave duration in II >than 2
and half small squares with
notched p wave
or
Negative component of
biphasic P wave in V1 ≥ 1 “small
box” in area

33. Right Atrial Enlargement
Criteria
P wave height in II >2 and
half small squares and are
also tall and peaked.
or
Positive component of
biphasic P wave in V1 > 1
“small box” in area

34. Slide 15

35. Atrial fibrillation
P
waves thrown into number of small
abnormal P waves before each QRS
complex
 The duration of R-R interval varies
 The amplitude of R-R varies
 Abnormal P waves don’t resemble one
another.

36. Slide 41

37. Atrial flutter
 The
P waves thrown into number of
abnormal P waves before each QRS
complex.
 But these abnormal P waves almost
resemble one another and are more
prominent like saw tooth appearance.

38. Slide 40

39. Junctional rhythm
 In
Junctional rhythm the P waves may be
absent or inverted.in next slide u can see
these inverted P waves.

40. Slide 43

41. Paroxysmal atrial tachycardia
 The
P and T waves you cant make out
separately
 The P and T waves are merged in one
 The R-R intervals do not vary but remain
constant and same.
 The heart rate being very high around 150
and higher.

42. Slide 39

43. NORMAL P-R INTERVAL
 PR
interval
seconds.
 That
time 0.12 seconds to 0.2
is three small squares to five small
squares.

44. 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

45. Short P-R interval
 Short
P-R interval seen in WPW syndrome or preexcitation syndrome or LG syndrome
 P-R interval is less than three small squares.
 The beginning of R wave slopes gradually up and
is slightly widened called Delta wave.
 There may be S-T changes also like ST depression
and T wave inversion.

46. Slide 17

47. Lengthening of P-R interval
 Occurs
in first degree heart block.
 The P-R interval is more than 5 small
squares or > than 0.2 seconds.
 This you will see in all leads and is same
fixed lengthening .

48. Slide 44

49. 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.

50. Normal Q wave

51. 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.

52. Q wave in MI

53. Q wave in septal hypertrophy

55. QRS COMPLEX
 QRS
duration <0.11 s
 That is less than almost three small squares
 Some books write 2 and a half small
squares.
 Height of R wave is (V1-V6) >8 mm some
say >10 mm chest leads (in at least one of
chest leads).

56. 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.

57. 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

58. 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

59. J point
 The
term J point means Junctional point at
the end of S wave between S wave and
beginning of S-T segment.

60. ST
Q
S
J point

61. L V H-Voltage Criteria
In adult with normal chest wall
SV1+RV5 >35 mm
or
SV1 >20 mm
or
RV6 >20 mm

62. Left ventricular
hypertrophy-Voltage
Criteria
 Count
small squares of downward R wave
in V1 plus small squares of R wave in V5 .
 If it comes to more than 35 small squares
then it is suggestive of LVH.

63. LEFT VENTRICULAR
HYPERTROPHY

64. Right ventricular hypertrophy
 Normally
you see R wave is downward
deflection in V1.but if you see upward R
wave in V1 then it is suggestive of RVH
etc.

65. Dominant or upward R wave
in V1
 Causes
 RBBB
 Chronic
lung disease, PE
Posterior MI
WPW Type A
Dextrocardia
Duchenne muscular dystrophy

66. Right Ventricular Hypertrophy
 WILL
SHOW AS
 Right axis deviation (RAD)
 Precordial leads
 In V1, R wave > S wave
 In V6, S wave > R wave
 Usual manifestation is pulmonary disease or
 congenital heart disease

68. Right Ventricular Hypertrophy

69. Right ventricular hypertrophy
 Right
ventricular hypertrophy (RVH)
increases the height of the R wave in V1.
And R wave in V1 greater than 7 boxes in
height, or larger than the S wave, is
suspicious for RVH. Other findings are
necessary to confirm the ECG diagnosis.

70. Right Ventricular Hypertrophy
 Other
findings in RVH include right axis
deviation, taller R waves in the right
precordial leads (V1-V3), and deeper S
waves in the left precordial (V4-V6). The T
wave is inverted in V1 (and often in V2).

71. Right Ventricular Hypertrophy
 True
posterior infarction may also cause a
tall R wave in V1, but the T wave is usually
upright, and there is usually some evidence
of inferior infarction (ST-T changes or Qs
in II, III, and F).

72. Right Ventricular Hypertrophy
A
large R wave in V1, when not
accompanied by evidence of infarction, nor
by evidence of RVH (right axis, inverted T
wave in V1), may be benign “counterclockwise rotation of the heart.” This can be
seen with abnormal chest shape.

73. Right Ventricular Hypertrophy
Although there is no widely accepted criteria for
detecting the presence of RVH, any combination of
the following EKG features is suggestive of its
presence:
 Tall
R wave in V1
 Right
axis deviation
 Right atrial enlargement
 Down sloping ST depressions in V1-V3 ( RV strain
pattern)

74. Right Ventricular Hypertrophy

75. Left Ventricular Hypertrophy

76. Left Ventricular Hypertrophy

77. ECG criteria for RBBB
 •(1)
QRS duration exceeds 0.12 seconds or
2 and half small squares roughly in V1 and
may also see it in V2.
 •(2) RSR complex in V1 may extend to V2.

78. ECG criteria for RBBB
 •ST/T
must be opposite in direction to the terminal
QRS(is secondary to the block and does not mean
primary ST/T changes).
 It
you meet all above criteria it is then complete
right bundle branch block.
 In incomplete bundle branch block the duration of
QRS will be within normal limits.

79. RBBB & MI
 If
abnormal Q waves are present they will
not be masked by the RBBB pattern.
 •This is because there is no alteration of the
initial part of the complex RS (in V1) and
abnormal Q waves can still be seen.

80. Significance of RBBB
 RBBB
is seen in : (1) occasional normal subjects
 (2) pulmonary embolus
 (3) coronary artery disease
 (4) ASD
 (5) active Carditis
 (6) RV diastolic overload

81. Partial / Incomplete RBBB
 is
diagnosed when the pattern of RBBB is
present but the duration of the QRS does
not exceed 0.12 seconds or roughly 2 and a
half small squares.

82. In next slide you will see
 ECG
characteristics of a typical RBBB
showing wide QRS complexes with a
terminal R wave in lead V1 and slurred S
wave in lead V6.
 Also you see R wave has become upright in
V1.QRS duration has also increased making
it complete RBBB.

83. 

84. ECG criteria for LBBB
 (1)Prolonged
QRS complexes, greater than 0.12
seconds or roughly 2 and half small squares in all
leads almost.
 (2)Wide, notched QRS (M shaped) V5, V6
 (3)Wide, notched QS complexes are seen in V1
(due to spread of activation away from the
electrode through septum + LV)
 (4)In V2, V3 small r wave may be seen due to
activation of para septal region

85. ECG criteria for LBBB
 So
look in all leads for QRS duration to
make it complete LBBB or incomplete
LBBB as u did in RBBB.
 Look in V5 and V6 for M shaped pattern at
summit or apex of R wave.
 Look for any changes as S-T depression and
T wave in inversion if any.

86. Significance of LBBB
 LBBB
is seen in : (1) Always indicative of organic heart disease
 (2) Found in ischemic heart disease
 (3) Found in hypertension.
 MI should not be diagnosed in the presence of
LBBB →Q waves are masked by LBBB pattern
 Cannot diagnose the presence of MI with LBBB

87. Partial / Incomplete LBBB
 is
diagnosed when the pattern of LBBB is
present but the duration of the QRS does
not exceed 0.12 seconds or roughly 2 and
half small squares.

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

93. NORMAL CONCAVITY OF S-T
SEGMENT
 It
then gradually slopes upwards making
concavity upwards and not going more
than one small square upwards from
isoelectric line or one small square below
isoelectric line.
 In MI this concavity may get lost and
become convex upwards called coving of
S-T segment.

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

95. Slide 11

96. Slide 12

97. Stress test ECG – note the ST Depression

99. Note the arrows pointing ST
depression

100. ST depression & Troponin T
positive is NON STEMI

101. Coving of S-T segment
 Concavity
upwards.
lost and convexity appear facing

102. Diagnostic criteria for AMI
•
•
•
•
•
Q wave duration of more than
0.04 seconds
Q wave depth of more than 25%
of ensuing r wave
ST elevation in leads facing
infarct (or depression in opposite
leads)
Deep T wave inversion overlying
and adjacent to infarct
Cardiac arrhythmias

103. Abnormalities of ST- segment

104. Q waves in myocardial
infarction

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

107. 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.
2.
Prolonged QT interval: hypocalcemia and
congenital long QT syndrome.
Short QT interval: hypercalcemia.

108. QT Interval
- Should be < 1/2 preceding R to
R interval -

109. QT Interval
- Should be < 1/2 preceding R to
R interval -
QT interval

110. QT Interval
- Should be < 1/2 preceding R to
R interval -
QT interval

111. QT Interval
- Should be < 1/2 preceding R to
R interval R
QT interval
R

112. QT Interval
- Should be < 1/2 preceding R to
R interval R
QT interval
R

113. QT Interval
- Should be < 1/2 preceding R to
R interval R
QT interval
R

114. QT Interval
- Should be < 1/2 preceding R to
R interval 65 - 90 bpm
R
QT interval
R

115. QT Interval
- Should be < 1/2 preceding R to
R interval 65 - 90 bpm
R
QT interval
Normal QTc = 0.46 sec
R

116. Atrioventricular (AV) Heart
Block

117. 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

118. AV Blocks
 First
Degree
– Prolonged AV conduction time
– PR interval > 0.20 seconds

119. 1st Degree AV Block
Prolongation of the PR interval, which is constant
All P waves are conducted

120. 1st degree AV Block:
• Regular Rhythm
• PRI > .20 seconds or 5 small squares and is CONSTANT
• Usually does not require treatment
PRI > .20 seconds

121. First Degree Block
prolonged PR interval

122. Analyze the Rhythm

123. AV Blocks
 Second
Degree
– Definition
 More Ps than QRSs
 Every QRS caused by a P

124. Second-Degree AV Block
 There
is intermittent failure of the supraventricular
impulse to be conducted to the ventricles
 Some
of the P waves are not followed by a QRS
complex.The conduction ratio (P/QRS ratio) may
be set at 2:1,3:1,3:2,4:3,and so forth


125. Second Degree
– Types
 Type I
– Wenckebach phenomenon

Type II
– Fixed or Classical

126. Type I Second-Degree AV
Block: Wenckebach
Phenomenon
 ECG
findings

1.Progressive lengthening of the PR
interval until a P wave is blocked

127. 2nd degree AV Block (“Mobitz I” also called “Wenckebach”):
• Irregular Rhythm
• PRI continues to lengthen until a QRS is missing (non-conducted sinus impulse)
• PRI is NOT CONSTANT
PRI = .24 sec
PRI = .36 sec
PRI = .40 sec
QRS is
“dropped”
Pause
4:3 Wenckebach (conduction ratio may not be constant)
Pattern Repeats………….

129. Type II Second-Degree AV
Block:
Mobitz Type II

ECG findings
1.Intermittent or unexpected blocked P waves
you don’t know when QRS drops

2.P-R intervals may be normal or prolonged,but
they remain constant

4. A long rhythm strip may help


131. Second Degree AV Block
Mobitz type I or Winckebach
Mobitz type II

132. Type 1
(Wenckebach)
Progressive prolongation of the PR interval until a P
wave is not conducted.
Type 2
Constant PR interval with unexpected intermittent failure to conduct

133. Mobitz Type I

134. MOBITZ TYPE 1

135. 2nd degree AV Block (“Mobitz II”):
• Irregular Rhythm
• QRS complexes may be somewhat wide (greater than .12 seconds)
• Non-conducted sinus impulses appear at unexpected irregular intervals
• PRI may be normal or prolonged but is CONSTANT and fixed
• Rhythm is somewhat dangerous May cause syncope or may deteriorate into complete heart
block (3rd degree block)
• It’s appearance in the setting of an acute MI identifies a high risk patient
• Cause: anterioseptal MI,
•Treatment: may require pacemaker in the case of fibrotic conduction system
PRI is CONSTANT
Non-conducted
sinus impulses
“2:1 block”
“3:1 block”

136. Analyze the Rhythm

137. Second Degree Mobitz
– Characteristics
– Atrial rate > Ventricular rate
– QRS usually longer than 0.12 sec
– Usually 4:3 or 3:2 conduction ratio (P:QRS ratio)

138. Analyze the Rhythm

139. Mobitz II


Definition: Mobitz II is characterized by 2-4 P
waves before each QRS. The PR pf the
conducted P wave will be constant for each QRS
. EKG Characteristics:Atrial and ventricular rate
is irregular. P Wave: Present in two, three or four
to one conduction with the QRS. PR Interval
constant for each P wave prior to the QRS. QRS
may or may not be within normal limits.

140. Mobitz Type II

141. Mobitz Type II
Sudden appearance of a single, nonconducted sinus P wave...

142. Advanced Second-Degree
AV Block
Two or more consecutive nonconducted sinus P
waves

143. Complete AV Block
– Characteristics
 Atrioventricular dissociation
 Regular P-P and R-R but without association
between the two
 Atrial rate > Ventricular rate
 QRS > 0.12 sec

144. 3rd Degree (Complete) AV Block
EKG Characteristics:
No relationship between P waves and QRS complexes
Relatively constant PP intervals and RR intervals
Greater number of P waves than QRS complexes

145. Complete heart block
P
waves are not conducted to the ventricles
because of block at the AV node. The P
waves are indicated below and show no
relation to the QRS complexes. They 'probe'
every part of the ventricular cycle but are
never conducted.

146. 3rd degree AV Block (“Complete Heart Block”) :
• Irregular Rhythm
• QRS complexes may be narrow or broad depending on the level of the block
• Atria and ventricles beat independent of one another (AV dissociation)
• QRS’s have their own rhythm, P-waves have their own rhythm
• May be caused by inferior MI and it’s presence worsens the prognosis
•Treatment: usually requires pacemaker
QRS intervals
P-wave intervals – note how the P-waves sometimes distort QRS
complexes or T-waves

147. Third-Degree (Complete) AV
Block

148. Third-Degree (Complete) AV
Block
The P wave bears no relation to the
QRS complexes, and the PR intervals
are completely variable

149. 30 AV Block








AV dissociation
atria and ventricles beating on their own
no relation between P’s & QRS’s
Atrial rate is different from ventricular
ventricular rate: 30-60 bpm
Rhythm is regular for both
QRS can be narrow or wide
depends on site of pacemaker!

150. Key points








Wenckebach
look for group beating & changing PR
Mobitz II
look for reg. atrial rhythm & consistent PR
3o block
atrial & ventricular rhythm regular
􀂾 rate is different!!!
no consistent PR

152. Left Anterior Fascicular Block

Left axis deviation , usually -45 to -90 degrees

QRS duration usually <0.12s unless coexisting RBBB

Poor R wave progression in leads V1-V3 and deeper S
waves in leads V5 and V6

There is RS pattern with R wave in lead II > lead III
S wave in lead III > lead II



QR pattern in lead I and AVL,with small Q wave
No other causes of left axis deviation

153. LBB
LPIF
Lead I
Left Anterior Hemiblock (LAHB):
1.
Left axis deviation (> -30 degrees) will be noted
and there will be a prominent S-wave in Leads
II, and III
1.
LASF
2.
Lead III
Lead AVF

154. Left Posterior Fascicular Block
 Right
axis deviation
 QR pattern in inferior leads (II,III,AVF)
small q wave
 RS patter in lead lead I and AVL(small R
with deep S)

155. Lead I
LBB
LPIF
Left Posterior Hemiblock (LPHB):
1.
1.
Right axis deviation and there will be a prominent
S-wave in Leads I. Q-waves may be noted in III
and AVF.
Notes on (LPHB):
•
QRS is normal width unless BBB is present
•
If LPHB occurs in the setting of an acute MI,
it is almost always accompanied by RBBB
and carries a mortality rate of 71%
LASF
2.
Lead III
Lead AVF

156. Bifascicular Bundle Branch
Block
RBBB with either left anterior or left posterior
fascicular block
 Diagnostic criteria
 1.Prolongation of the QRS duration to 0.12 second
or longer
 2.RSR’ pattern in lead V1,with the R’ being broad
and slurred
 3.Wide,slurred S wave in leads I,V5 and V6
 4.Left axis or right axis deviation


157. Trifascicular Block
 The
combination of RBBB, LAFB and long
PR interval
 Implies
that conduction is delayed in the
third fascicle

158. Indications For Implantation of
Permanent Pacing in Acquired AV
Blocks




1.Third-degree AV block, Bradycardia with symptoms
Asystole
e.Neuromuscular diseases with AV block (Myotonic
muscular dystrophy)
2.Second-degree AV block with symptomatic bradycardia

159. Cardiac Pacemakers
 Definition
– Delivers artificial stimulus to heart
– Causes depolarization and contraction
 Uses
– Bradyarrhythmias
– Asystole
– Tachyarrhythmias (overdrive pacing)

160. Cardiac Pacemakers
 Types
– Fixed



Fires at constant rate
Can discharge on T-wave
Very rare
– Demand


Senses patient’s rhythm
Fires only if no activity sensed after preset interval (escape
interval)
– Transcutaneous vs Transvenous vs Implanted

161. Cardiac Pacemakers

162. Cardiac Pacemakers
 Demand
Pacemaker Types
– Ventricular
 Fires ventricles
– Atrial
Fires atria
 Atria fire ventricles
 Requires intact AV conduction


163. Cardiac Pacemakers
 Demand
Pacemaker Types
– Atrial Synchronous
 Senses atria
 Fires ventricles
– AV Sequential
Two electrodes
 Fires atria/ventricles in sequence


164. Cardiac Pacemakers
 Problems
– Failure to capture
 No response to pacemaker artifact
 Bradycardia may result
 Cause: high “threshold”
 Management
– Increase amps on temporary pacemaker
– Treat as symptomatic bradycardia

165. Cardiac Pacemakers
 Problems
– Failure to sense
 Spike follows QRS within escape interval
 May cause R-on-T phenomenon
 Management
– Increase sensitivity
– Attempt to override permanent pacer with temporary
– Be prepared to manage VF

166. Implanted Defibrillators

AICD
– Automated
Implanted CardioDefibrillator

Uses
– Tachyarrhythmias
– Malignant
arrhythmias


VT
VF

167. Implanted Defibrillators
 Programmed
at insertion to deliver predetermined
therapies with a set order and number of therapies
including:
– pacing
– overdrive pacing
– cardioversion with increasing energies
– defibrillation with increasing energies
– standby mode

Effect of standby mode on Paramedic treatments

168. Implanted Defibrillators
 Potential
Complications
– Fails to deliver therapies as intended


worst complication
requires Paramedic intervention
– Delivers therapies when NOT appropriate


broken or malfunctioning lead
parameters for delivery are not specific enough
– Continues to deliver shocks


parameters for delivery are not specific enough and device
senses a reset
may be shut off (not standby mode) with donut-magnet

169. Sinus Exit Block
 Due
to abnormal function of SA node
 MI, drugs, hypoxia, vagal tone
 Impulse blocked from leaving SA node
 usually transient
 Produces 1 missed cycle
 can confuse with sinus pause or arrest

170. Sinus block

171. ARRTHYMIAS AND
ECTOPIC BEATS

172. Recognizing and Naming Beats & Rhythms
Atrial Escape Beat
QRS is slightly different but still narrow,
indicating that conduction through the
ventricle is relatively normal
normal ("sinus") beats
sinus node doesn't fire leading
to a period of asystole (sick
sinus syndrome)
p-wave has different shape
indicating it did not originate in
the sinus node, but somewhere
in the atria. It is therefore called
an "atrial" beat

173. Recognizing and Naming Beats & Rhythms
Junctional Escape Beat
QRS is slightly different but still narrow,
indicating that conduction through the
ventricle is relatively normal
there is no p wave, indicating that it did
not originate anywhere in the atria, but
since the QRS complex is still thin and
normal looking, we can conclude that the
beat originated somewhere near the AV
junction. The beat is therefore called a
"junctional" or a “nodal” beat

174. Recognizing and Naming Beats & Rhythms
Ventricular
Escape Beat
QRS is wide and much different ("bizarre") looking
than the normal beats. This indicates that the beat
originated somewhere in the ventricles and
consequently, conduction through the ventricles did
not take place through normal pathways. It is
therefore called a “ventricular” beat
there is no p wave, indicating that the beat
did not originate anywhere in the atria
actually a "retrograde p-wave may sometimes be
seen on the right hand side of beats that
originate in the ventricles, indicating that
depolarization has spread back up through the
atria from the ventricles

175. The “Re-Entry” Mechanism of Ectopic Beats & Rhythms
Electrical Impulse
Cardiac
Conduction
Tissue
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
Tissues with these type of circuits may exist:
• in microscopic size in the SA node, AV node, or any type of heart tissue
• in a “macroscopic” structure such as an accessory pathway in WPW

176. The “Re-Entry” Mechanism of Ectopic Beats & Rhythms
Premature Beat Impulse
Cardiac
Repolarizing Tissue
Conduction
(long refractory period)
Tissue
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
1. An arrhythmia is triggered by a premature beat
2. The beat cannot gain entry into the fast conducting
pathway because of its long refractory period and
therefore travels down the slow conducting pathway only

177. The “Re-Entry” Mechanism of Ectopic Beats & Rhythms
Cardiac
Conduction
Tissue
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
3. The wave of excitation from the premature beat
arrives at the distal end of the fast conducting
pathway, which has now recovered and therefore
travels retrogradely (backwards) up the fast
pathway

178. The “Re-Entry” Mechanism of Ectopic Beats & Rhythms
Cardiac
Conduction
Tissue
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
4. On arriving at the top of the fast pathway it finds the
slow pathway has recovered and therefore the wave of
excitation ‘re-enters’ the pathway and continues in a
‘circular’ movement. This creates the re-entry circuit

179. Recognizing and Naming Beats & Rhythms
Premature Ventricular Contractions (PVC’s, VPB’s, extrasystoles) :
• A ventricular ectopic focus discharges causing an early beat
• Ectopic beat has no P-wave (maybe retrograde), and QRS complex is "wide and bizarre"
• QRS is wide because the spread of depolarization through the ventricles is abnormal (aberrant)
• In most cases, the heart circulates no blood (no pulse because of an irregular squeezing motion
• PVC’s are sometimes described by lay people as “skipped heart beats”
R on T
phenom em on
M u lt if o c a l
P V C 's
C o m p e n s a to ry p a u s e
a fte r th e o c c u r a n c e o f a P V C

180. Recognizing and Naming Beats & Rhythms
Characteristics of PVC's
• PVC’s don’t have P-waves unless they are retrograde (may be buried in T-Wave)
• T-waves for PVC’s are usually large and opposite in polarity to terminal QRS
• Wide (> .16 sec) notched PVC’s may indicate a dilated hypokinetic left ventricle
• Every other beat being a PVC (bigeminy) may indicate coronary artery disease
• Some PVC’s come between 2 normal sinus beats and are called “interpolated” PVC’s
The classic PVC – note the
compensatory pause
Interpolated PVC – note the sinus
rhythm is undisturbed

181. Recognizing and Naming Beats & Rhythms
PVC's are Dangerous When:
• They are frequent (> 30% of complexes) or are increasing in frequency
• The come close to or on top of a preceding T-wave (R on T)
• Three or more PVC's in a row (run of V-tach)
• Any PVC in the setting of an acute MI
• PVC's come from different foci ("multifocal" or "multiformed")
These dangerous phenomenon may preclude the occurrence of deadly arrhythmias:
• Ventricular Tachycardia
• Ventricular Fibrillation
The sooner defibrillation takes place,
the increased likelihood of survival
“R on T phenomenon”
time
sinus beats
V-tach
Unconverted V-tach r V-fib

182. Recognizing and Naming Beats & Rhythms
Notes on V-tach:
• Causes of V-tach
• Prior MI, CAD, dilated cardiomyopathy, or it may be idiopathic (no known cause)
• Typical V-tach patient
• MI with complications & extensive necrosis, EF<40%, d wall motion, v-aneurysm)
•V-tach complexes are likely to be similar and the rhythm regular
• Irregular V-Tach rhythms may be due to to:
• breakthrough of atrial conduction
• atria may “capture” the entire beat beat
• an atrial beat may “merge” with an ectopic ventricular beat (fusion beat)
Fusion beat - note pwave in front of PVC and
the PVC is narrower than
the other PVC’s – this
indicates the beat is a
product of both the sinus
node and an ectopic
ventricular focus
Capture beat - note that
the complex is narrow
enough to suggest normal
ventricular conduction.
This indicates that an
atrial impulse has made it
through and conduction
through the ventricles is
relatively normal.

183. Recognizing and Naming Beats & Rhythms
Premature Atrial Contractions (PAC’s):
• An ectopic focus in the atria discharges causing an early beat
• The P-wave of the PAC will not look like a normal sinus P-wave (different morphology)
• QRS is narrow and normal looking because ventricular depolarization is normal
• PAC’s may not activate the myocardium if it is still refractory (non-conducted PAC’s)
• PAC’s may be benign: caused by stress, alcohol, caffeine, and tobacco
• PAC’s may also be caused by ischemia, acute MI’s, d electrolytes, atrial hypertrophy
• PAC’s may also precede PSVT
PAC
Non conducted PAC
Non conducted PAC
distorting a T-wave

184. Recognizing and Naming Beats & Rhythms
Premature Junctional Contractions (PJC’s):
• An ectopic focus in or around the AV junction discharges causing an early beat
• The beat has no P-wave
• QRS is narrow and normal looking because ventricular depolarization is normal
• PJC’s are usually benign and require not treatment unless they initiate a more serious rhythm
PJC

185. Recognizing and Naming Beats & Rhythms
Multifocal Atrial Tachycardia (MAT):
• Multiple ectopic focuses fire in the atria, all of which are conducted normally to the ventricles
• QRS complexes are almost identical to the sinus beats
• Rate is usually between 100 and 200 beats per minute
• The rhythm is always IRREGULAR
• P-waves of different morphologies (shapes) may be seen if the rhythm is slow
• If the rate < 100 bpm, the rhythm may be referred to as “wandering pacemaker”
• Commonly seen in pulmonary disease, acute cardiorespiratory problems, and CHF
• Treatments: Ca++ channel blockers,  blockers, potassium, magnesium, supportive therapy for
underlying causes mentioned above (antiarrhythmic drugs are often ineffective)
Note different P-wave
morphologies when the
tachycardia begins
Note IRREGULAR
rhythm in the tachycardia

186. Recognizing and Naming Beats & Rhythms
Paroxysmal (of sudden onset) Supraventricular Tachycardia (PSVT) :
• A single reentrant ectopic focuses fires in and around the AV node, all of which are conducted
normally to the ventricles (usually initiated by a PAC)
• QRS complexes are almost identical to the sinus beats
• Rate is usually between 150 and 250 beats per minute
• The rhythm is always REGULAR
• Possible symptoms: palpitations, angina, anxiety, polyuruia, syncope (d Q)
• Prolonged runs of PSVT may result in atrial fibrillation or atrial flutter
• May be terminated by carotid massage
• u carotid pressure r u baroreceptor firing rate r u vagal tone r d AV conduction
• Treatment: ablation of focus, Adenosine (d AV conduction), Ca++ Channel blockers
Rhythm usually begins
with PAC
Note REGULAR rhythm
in the tachycardia

187. Sinus arrest or exit block

188. PAC

189. 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)

190. Junctional Escape Beat

191. Junctional Rhythm
 Rate:
40 to 60 beats/minute (atrial and ventricular)
 •Rhythm: regular atrial and ventricular rhythm
 •P wave: usually inverted, may be upright; may
precede,
 follow or be hidden in the QRS complex; may
 be absent
 •PR interval: not measurable or less than .20 sec.

192. Junctional Rhythm

193. MaligMalignant PVC
patterns
 Frequent
PVCs
Multiform PVCs
 Runs of consecutive PVCs
 R on T phenomenon – PVC that falls on a T
 wave
 PVC during acute MI

196. Types of PVCs
 Uniform
Multiform
 PVC rhythm patterns
 – Bigeminy – PVC occurs every other
complex
 – Couplets – 2 PVCs in a row
 – Trigeminy – Two PVCs for every three
complexes


197. Junctional Escape Rhythm

198. Ventricular tachycardia
(VTach)
3
or more PVCs in a row at a rate of 120 to
200 bts/min-1
Ventricular fibrillation (VFib)
 No visible P or QRS complexes. Waves
appear as fibrillating waves

200. Torsades de Pointes
 Type
of VT known as “twisting of the
points.”
 Usually seen in those with prolonged QT
intervals caused by

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

202. Atrial Fibrillation:

203. Regular “Irregular”
Premature
Beats: PVC
– Widened QRS, not associated with
preceding P wave
– Usually does not disrupt P-wave
regularity
– T wave is “inverted” after PVC
– Followed by compensatory
ventricular pause

204. Notice a Pattern in the PVC’s?

205. Identifying AV Blocks:
Name
1°:
Conduction
P=R
PR-Int
> .20
R-R Rhythm
Regular
2°:Mobitz P > R
I
Progressive Irregular
2°:Mobitz P > R
II
Constant
Regular
3°:
Grossly
Irregular
Regular
P>R
(20-40 bpm)

206. Most Important Questions
of Arrhythmias

What is the mechanism?
– Problems in impulse formation?
(automaticity or ectopic foci)
– Problems in impulse
conductivity? (block or re-entry)
 Where
is the origin?
– Atria, Junction, Ventricles?

207. QRS Axis
Check Leads:
1 and AVF

208. Interpreting Axis
Deviation:
 Normal
Electrical Axis:
– (Lead I + / aVF +)
 Left
Axis Deviation:
– Lead I + / aVF –
– Pregnancy, LV hypertrophy etc
 Right
Axis Deviation:
– Lead I - / aVF +
– Emphysema, RV hypertrophy etc.

209. NW Axis (No Man’s Land)
Both
I and aVF are –
Check to see if leads are
transposed (- vs +)
Indicates:
– Emphysema
– Hyperkalemia
– VTach

210. Determining Regions of
CAD: ST-changes in leads…
RCA:
Inferior myocardium
– II, III, aVF
LCA:
Lateral myocardium
– I, aVL, V5, V6
LAD:
Anterior/Septal
myocardium
– V1-V4

211. Regions of the
Myocardium:
Lateral
I, AVL,
V5-V6
Inferior
II, III, aVF
Anterior /
Septal
V1-V4

212. Sinus Arrhythmia

213. Sinus Arrest/Pause

214. Sinoatrial Exit Block

215. Premature Atrial Complexes
(PACs)

216. Wandering Atrial Pacemaker
(WAP)

217. Supraventricular Tachycardia
(SVT)

218. Wolff-Parkinson-White
Syndrome (WPW)

219. Atrial Flutter

220. Atrial Fibrillation
(A-fib)

221. Premature Junctional
Complexes (PJC)

222. Junctional Rhythm

223. Junctional Rhythm

224. Accelerated Junctional Rhythm

225. Junctional Tachycardia

226. Premature Ventricular
Complexes (PVC's)
Note – Complexes not
Contractions

227. PVC’s
 Uniformed/Multiformed
 Couplets/Salvos/Runs
 Bigeminy/Trigeminy/Quadrageminy

228. Uniformed PVC’s

229. R on T Phenomena

230. Multiformed PVC’s

231. PVC Couplets

232. PVC Salvos and Runs

233. Bigeminy PVC’s

234. Trigeminy PVC’s

235. Quadrageminy PVC’s

236. Ventricular Escape Beats

237. Idioventricular Rhythm

238. Ventricular Tachycardia (VT)
 Rate:
101-250 beats/min
 Rhythm:
P
regular
waves: absent
 PR
interval: none
 QRS
duration: > 0.12 sec. often difficult to
differentiate between QRS and T wave
Note: Monomorphic - same shape
and amplitude

239. Ventricular Tachycardia (VT)

240. V Tach

241. Torsades de Pointes (TdeP)
 Rate:
150-300 beats/min
 Rhythm:
P
regular or irregular
waves: none
 PR
interval: none
 QRS
duration: > 0.12 sec. gradual alteration
in amplitude and direction of the QRS
complexes

242. Torsades de Pointes (TdeP)

243. Ventricular Fibrillation (VF)
 Rate:
CNO as no discernible complexes
 Rhythm:
P
rapid and chaotic
waves: none
 PR
interval: none
 QRS
duration: none
Note: Fine vs. coarse?

244. Ventricular Fibrillation (VF)

245. Ventricular Fibrillation (VF)

246. Asystole
(Cardiac Standstill)
 Rate:
none
 Rhythm:
P
none
waves: none
 PR
interval: not measurable
 QRS
duration: absent

247. Asystole
(Cardiac Standstill)

248. Asystole
The Mother of all Bradycardias

249. Atrial Pacemaker
(Single Chamber)
pacemaker
•Capture?

250. Ventricular Pacemaker
(Single Chamber)
pacemaker

251. Dual Paced Rhythm
pacemaker

252. Pulseless Electrical Activity
(PEA)
 The
absence of a detectable pulse and blood
pressure
 Presence
of electrical activity of the heart as
evidenced by ECG rhythm, but not VF or VT
+
= 0/0 mmHg

253. ventricular bigeminy
 The
ECG trace below shows
ventricular bigeminy, in which
every other beat is a ventricular
ectopic beat. These beats are
premature, wider, and larger than
the sinus beats.

254. ventricular bigeminy

255. ventricular trigeminy;
 The
occurrence of more than one
type of ventricular ectopic impulse
morphology is evidence of
multifocal ventricular ectopics. In
this example, the ventricular
ectopic beats are both wide and
premature, but differ considerably
in shape

256. ventricular trigeminy

257. ventricular trigeminy

258. MYOCARDIAL
INFARACTION

259. 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

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

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

262. Anterior Myocardial Infarction
If you see changes in leads V1 - V4 that
are consistent with a myocardial
infarction, you can conclude that it is an
anterior wall myocardial infarction.

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

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

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

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

267. Putting it all Together
How about now?

268. Anterolateral MI
This person’s MI involves both the anterior wall (V2V4) and the lateral wall (V5-V6, I, and aVL)!

269. I II III
aVR aVL aVF
V1 V2 V3
V4 V5 V6
The ST segment should start isoelectric except in V1
and V2 where it may be elevated

270. Characteristic changes in AMI





ST segment elevation over area of damage
ST depression in leads opposite infarction
Pathological Q waves
Reduced R waves
Inverted T waves

271. ST elevation hyperacute
phase
• Occurs in the early stages
R
ST
P
Q
• Occurs in the leads facing
the infarction
• Slight ST elevation may be
normal in V1 or V2

272. Deep Q wave
• Only diagnostic change of
myocardial infarction
R
ST
• At least 0.04 seconds in
duration
P
T
Q
• Depth of more than 25% of
ensuing R wave

273. T wave changes
• Late change
R
• Occurs as ST elevation
is returning to normal
ST
P
• Apparent in many leads
T
Q

274. Bundle branch block
Anterior wall MI
I II III
aVR aVL aVF
V1 V2 V3
Left bundle branch block
V4 V5 V6
I II III
aVR aVL aVF
V1 V2 V3
V4 V5 V6

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

276. Anterior infarction
Anterior infarction
I II III
Left
coronary
artery
aVR aVL aVF
V1 V2 V3
V4 V5 V6

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

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

279. Diagnostic criteria for AMI
•
•
•
•
•
Q wave duration of more than
0.04 seconds
Q wave depth of more than 25%
of ensuing r wave
ST elevation in leads facing
infarct (or depression in opposite
leads)
Deep T wave inversion overlying
and adjacent to infarct
Cardiac arrhythmias

280. Surfaces of the Left Ventricle

Inferior - underneath

Anterior - front

Lateral - left side

Posterior - back

281. Inferior Surface


Leads II, III and avF look UP from below to the inferior
surface of the left ventricle
Mostly perfused by the Right Coronary Artery

282. Inferior Leads
– II
– III
– aVF

283. Anterior Surface



The front of the heart viewing the left ventricle and the
septum
Leads V2, V3 and V4 look towards this surface
Mostly fed by the Left Anterior Descending branch of the
Left artery

284. Anterior Leads
– V2
– V3
– V4

285. Lateral Surface



The left sided wall of the left ventricle
Leads V5 and V6, I and avL look at this surface
Mostly fed by the Circumflex branch of the left artery

286. Lateral Leads
V5, V6,
I, aVL

287. Posterior Surface



Posterior wall infarcts are rare
Posterior diagnoses can be made by looking at the anterior
leads as a mirror image. Normally there are inferior
ischaemic changes
Blood supply predominantly from the Right Coronary
Artery

288. RIGHT
Inferior
II, III, AVF
Posterior
V1,
V2, V3
LEFT
Antero-Septal
V1,V2, V3,V4
Lateral
I, AVL, V5,
V6

289. ST Segment Elevation
The ST segment lies above the isoelectric line:
 Represents
myocardial injury
 It is the hallmark of Myocardial Infarction
 The injured myocardium is slow to repolarise and
remains more positively charged than the
surrounding areas
 Other causes to be ruled out include pericarditis
and ventricular aneurysm

290. ST-Segment Elevation

292. T wave inversion in an
evolving MI

293. The ECG in ST Elevation MI

294. The Hyper-acute Phase
Less than 12 hours




“ST segment elevation is the hallmark ECG abnormality
of acute myocardial infarction” (Quinn, 1996)
The ECG changes are evidence that the ischaemic
myocardium cannot completely depolarize or repolarize as
normal
Usually occurs within a few hours of infarction
May vary in severity from 1mm to ‘tombstone’ elevation

296. The Fully Evolved Phase
24 - 48 hours from the onset of a myocardial infarction
 ST segment elevation is less (coming back to baseline).
 T waves are inverting.
 Pathological Q waves are developing (>2mm)

297. The Chronic Stabilised Phase
 Isoelectric
ST segments
 T waves upright.
 Pathological Q waves.
 May take months or weeks.

299. Reciprocal Changes
 Changes
occurring on the opposite side of
the myocardium that is infarcting

300. Reciprocal Changes ie S-T
depression in some leads in
MI

301. Non ST Elevation MI
 Commonly
ST depression and deep T wave
inversion
 History of chest pain typical of MI
 Other autonomic nervous symptoms present
 Biochemistry results required to diagnose
MI
 Q-waves may or may not form on the ECG

302. Changes in NSTEMI

303. + + + +
_ _ _ _
_
_ _ _ _
+ + + +
+
+
+
+
+ _
+ __
+
+
Action potentials and
electrophysiology
+
Na
_ _ _ _ _
_
_
+ + + + +
_ +
+ _
_ + + + + + _
_ _ _ _ _
+
_
_
_ + + + + + _
+
+
_ + + + + + _
_ _ _ _ _
+
K
_ _ _ _ _
+
+ _
_
+
_
+
+
+ + + +
_ _ _ _
_
_ _ _ _
+ + + +
+
+
+
K
Resting
Depolarised
Ca
+
Na
++
in(slow)
in
K
++
Ca
+
out
Plateau
Repolarised
3.2

304. LVH and strain pattern
Ventricular Strain
Strain is often associated with ventricular hypertrophy
Characterized by moderate depression of the ST segment.

305. Non-ischaemic ST segment changes: in patient taking digoxin (top)
and in patient with left ventricular hypertrophy (bottom)
Channer, K. et al. BMJ 2002;324:1023-1026
Copyright ©2002 BMJ Publishing Group Ltd.

306. Examples of T wave
abnormalities
Copyright ©2002 BMJ Publishing Group Ltd.
Channer, K. et al. BMJ 2002;324:1023-1026

307. 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

308. Bundle Branch Block

309. Left Bundle Branch Block
 Widened
QRS (> 0.12 sec, or 3 small
squares)
 Two R waves appear – R and R’ in V5 and
V6, and sometimes Lead I, AVL.
 Have predominately negative QRS in V1,
V2, V3 (reciprocal changes).

310. Right Bundle Branch Block

311. Where’s the MI?

312. Where’s the MI?

313. Where’s the MI?

314. Final one…

316. Which one is more
tachycardic during this
exercise test?

317. Any Questions?

318. I hope you have found this
session useful.