.....

2. Content:
RRA:
RHYTHM ,
RATE , AXIS
NORMAL
ECG
RHYTHM
ABNORMALITIES
ABNORMALITIES
OF P-R
DISEASES OF
ATRIA &
VENTRICLE
BUNDLE BRANCH
BLOCK
INFARCTIONS
OTHER CASES
QUIZZES

3. Normal
ECG
1

4. Normal Intervals

5. Notes :
 Q wave is always negative
with the exception of lead 3
and aVR .
 Abnormal (pathological)
Q-wave is more than 0.04
second "one small box' in
duration OR more than one
third the height of the
following R-wave.

6. R
RHYTHM
R
RATE
A
AXIS

7. Rhythm
 Sinus or not
 Regular or not

8. Rate
 regular
𝟑𝟎𝟎
number of large squares
between R−R interval

9. Rate
 irregular
20 × number of QRS
complexes in 15 large squares

10. Axis
We have many ways but the simplest one
is:
 Look for lead 1 and lead 3 , if both QRS
complexes are predominantly upward ,
this mean normal axis
 If QRS complexes in lead 1 is downward
and in lead 2 and 3 are upward , this mean
RAD
 IF QRS complexes in lead 1 is upward and in
lead 2 and 3 are downward , this mean
LAD

11. Normal
Axis
RAD
LAD
Lead 1 Lead 2 Lead 3

12. RAD

13. LAD

14. 


CAUSES

15. Rhythm
Abnormalities

16. Some pathological causes :
* MI * Hypothermia
* Cholestatic jaundice * Hypothyroidism
* Drugs , eg. B-blockers , digoxin , verapamil
1 Sinus bradycardia

17. Treatment : “ACLS”
Is the patient hemodynamically stable or not?
YES
Monitor &
observe
NO
* Give ATROPINE 0.5 mg IV push to
repeat every 3-5 minutes
If it is ineffective , the next options
will be :
* DOPAMIN infusion 2-20 mcg /kg/
min
EPINEPHRINE infusion 2-10 mcg/
* Transcutaneous pacing

18. *Anxiety *Fever *Anemia
*Heart failure *Thyrotoxicosis
*Phaeochromocytoma *Drugs , eg, B-agonist
Some pathological causes :
2 Sinus tachycardia

19. Treatment : “ACLS”

20. 3 Sinus Arrhythmia
It is a normal phenomenon that occurs with changes
in intrathoracic pressure .The heart rate increase
with inspiration (R-R interval shorten) and decreases
with expiration (R-R interval lengthen) ,
so the rhythm is irregular

21. Supraventricular Tachycardia
(SVT )
ECG Characteristics :
* Absent P wave , they are often
hidden in the QRS complex
* Rhythm : regular
* Rate : 150 – 250
* QRS complex : NARROW
4

22. The most common type is
atrioventricular nodal
reentrent tachycardia 'AVNRT'

23. Another example of SVT :
Narrow complex tachycardia ~ 220 bpm.
No visible P waves.

24. Another example of SVT :

25. Treatment of SVT
Is the patient hemodynamically stable or not?
NO
Synch.
DC
YES
Measures to ↑ vagal tone:
A:press on eyeball
B:carotid sinus massage
C:Valsalva maneuver
D:immersing the face in cold
water
NO
EFFECT
IV
ADENOSIN
NO EFFECT
B BLOCKER
CCB
Digoxin
NO
EFFECT
ALTERNATIVE CLASSES :
CLASS 1 A
CLASS 1 C
CLASS 3

26. Ventricular Tachycardia
(VT )
ECG Characteristics :
*P-wave : usually not seen
*Rhythm :regular
*Rate : 101 – 250
*QRS complex : WIDE
5

27. A ) Monomorphic VT
The QRS complexes are of the
same shape and amplitude
Its like
number
7
or
8
in
Arabic

28. B ) Polymorphic VT
The QRS complexes vary in shape

29. Treatment of VT
Is the patient hemodynamically stable or not?
NO
Synch.
DC
YES
* AMIODARONE
300 mg IV over
10-20 min
* IV LIDOCAINE
Always treat :
Hypokalemia
Hypomagnesaemia
Acidosis
Hypoxemia

30. NOTES :
For prevention of VT : give B blocker
( Amiodarone can be added if additional control
is needed )
CLASS 1C anti arrhythmic drugs ( flecainide ,
propafenone ) should not be used for
prevention of VT in patient with coronary
artery disease or heart failure .
In patients at high risk of arrhythmic
death , the use of implantable cardiac
defibrillator is recommended.

31. 6 Atrial fibrillation
'AF'
ECG Characteristics
* P-wave : not seen
Rhythm : usually*
irregularly irregular

32. Some causes :
* Coronary artery disease * Hypertension
* Valvular heart disease * Hyperthyroidism
* Cardiomyopathy * Alcohol

33. Another example of AF :

34. Another example of AF :

35. Treatment of AF
Full history
Examination
12 lead ECG
Measure the vital signs
Is the patient hemodynamically stable or not?
NO
Synch.
DC
YES
B BLOCKER
CCB
DIGOXIN
ADENOSIN
AV node blocking agents :
{1st choice in general
→1st choice if there is heart
failure
Continue-

36. Then ask about the duration of the symptoms :
Less than
48 hrs.
more than
48 hrs.
We give a
cardioverter
drug , either
CLASS 1C OR
CLASS 3
The patient may have a thrombus ,
so we should exclude it by
trans esophageal echo OR we put the
patient on anticoagulation for 4
weeks THEN do cardioversion
THEN we keep the patient on
anticoagulation for at least 3 months
following successful cardioversion.

37. 7 Atrial Flutter
ECG Characteristics :
* P-wave : not identifiable
, with saw toothed , flutter
waves In :
lead 2 , lead 3 , aVF & V1.
* Rhythm : usually regular

38. NOTE : the atrial rate usually range from
220 – 430 bpm .
the ventricular rate is half of the atrial rate.

39. Another example of Atrial Flutter :

40. Treatment of Atrial Flutter
Is the patient hemodynamically stable or not?
NO
Synch.
DC
YES
AV node blocking
agents :
B BLOCKER
CCB
DIGOXIN
ADENOSIN
Alternative
classes :
CLASS 1C
CLASS 3
We should give anticoagulation depend on
CHADSVAS SCORE & like that of
Af as we mentioned.

41. abnormalities
of
P-R
interval
4

42. A
SHORT P-R INTERVAL
Example
Wolf–Parkinson–White
(WPW) syndrome

43. ECG characteristics of WPW :
* Short P-R interval , less than 3
squares
*Slurring of the QRS complexes ,
Called Delta wave
* Sometimes wide QRS complexes

44. WPW may be described as type A or B
Type A
Type A has a positive delta wave & there is
prominent R in V1

45. Type B
There is prominent R in V5 & V6 but the R is
negative in V1

46. Notes :
• Usually The presentation of WPW is
Either SVT or very rapid AF .
( if SVT the carotid sinus message or
IV adenosine can terminate the tachycardia
WHILE the very rapid AF may cause
collapse , syncope and even sudden
death so it should be treated as
emergency usually with DC cardioversion).
• Usually we can not diagnose WPW
During the attack of SVT or AF
unless we convert The tachyarrhythmia
to sinus rhythm .

47. • The drugs that contraindicated during
the attack of tachyarrhythmia :
1) IV digoxin
2) iv Beta blocker
3) IV CCB
• Prophylactic anti arrhythmic drugs
such as Flecainide or Propafenone , can
be used to slow conduction ,
and prolong the refractory period
of the accessory pathway .

48. B
LONG P-R INTERVAL
Example
:Heart block

49. 1st degree heart block
ECG characteristics :
* Rate : usually within normal range ,
but depends on the underlying rhythm
* PR interval : prolonged more than
0.20 sec ( more than 5 small squares)
but constant.

50. Causes :
1 : drugs : eg, B Blockers , CCB , digoxin
2 : degenerative changes in AV node
3 : acute inferior MI
RX : Usually it need no treatment

51. 2nd degree heart block
type 1 (Wenckebach , Mobitz type 1)
There is a progressive increase in
PR interval ,
until a P wave appears
without a QRS complex , then the
cycle is repeated.

52. RX : need no treatment

53. Another example of Wenckebach cycle :
Note the difference in PR interval between the first and last
QRS complex of each group.

54. Mobitz type 2
ECG characteristics :
The PR interval of the conducted
impulses remain constant but some P
waves not followed by QRS complexes

55. RX : This type of block is more serious and is
often progress to third degree heart block , so it
should be treated with temporary pacemaker.

56. Another example of Mobitz type 2 :

57. 3rd degree heart block
ECG characteristics :
*AV dissociation ( the atria and
ventricles beat independently )
* The Rate is slow ( 25-50 /min ).

58. CAUSES:
*A: Congenital
*B: Acquired, like :
*1:Idiopathic fibrosis *2:MI / Ischemia
*3:Drugs (eg digoxin)
*4 : Inflammation(eg,Chagas disease)
Rx :
pacemaker

59. 3rd degree heart block.

60. 5 Diseases
of
Atria &
ventricles

61. 1
P Pulmonale
* Tall , peaked wave greater than
2.5 mm in height in leads 2,3,aVF an
d large posterior initial
Positive deflection of the p wave in
V1.
*It indicate RA hypertrophy due to
any causes like tricuspid valve
stenosis OR pulmonary
hypertension

62. 2
P mitrale
＊Broad , notched and greater than 0.11
sec in duration , best see in lead 2 & V1
* Indicate LA hypertrophy or enlargement
＊It called P mitrale because of the mitral
valve disease (mitral stenosis ,
mitral regurgitation)
that are associated with this condition ,
but it generally
indicate LA hypertrophy.

64. ECG FEATURES :
*Right axis deviation
*Tall R in V1 , V2
(greater than 7 mm )
*Deep S wave in V6
3 Right
Ventricular
Hypertrophy

65. RVH

66. ECG FEATURES :
*left axis deviation
*The sum of S wave in V1 & R
wave in V5 or V6 is ˃ 35 mm
(7 large squares) .
OR R wave in aVL ˃ 11 mm
4 Left
Ventricular
Hypertrophy

67. LVH

68. Bundle
branch block
'BBB'
6

69. Right BBB Left BBB
*Normal variant
*Right ventricular
hypertrophy
*Congenital heart
Disease (eg. ASD )
*Coronary artery
disease
*Coronary
artery disease
*Hypertension
*Aortic valve
disease
*Cardiomyopathy
causes

70. ECG features of BBB:
Both of them had wide QRS complex ≥ 3 small
squares
LBBB RBBB
 Look to the left
leads ( lead1 , aVL ,
V5 & V6 ) , we will find
wide & slurred R wave.
 While in the right leads
(V1 &V2) , we will see
normal R wave but there
is wide & slurred S wave .
 Look to the right
leads (V1 &V2) , we
will find wide R with
rSR pattern .
 While in the left leads
( lead1 , aVL ,V5 & V6 ) , we will
see normal R wave but
there is Deep S .

71. LBBB
Dominant S wave in V1 with broad, notched (‘M’-shaped) R wave in V6

72. AF with LBBB

73. RBBB
Tall R’ wave in V1 (“M” pattern) with wide, slurred S wave in V6 (“W” pattern)

74. 6Infarctions

75. 1
2
Non – ST – Elevation MI
OR
Unstable angina
ST – Elevation MI
ECG changes : ST depression and / or
T wave inversion . We should differentiate
between them by the cardiac enzymes.
Acute coronary syndrome

76. ECG changes of STEMI according to
the time of appearance:
1 : Tented T wave
2 : ST elevation (convex )
3 : reduction of R wave
4 : pathological Q wave
5 : deep T wave inversion

77. LocalizationLeads Coronary
artery
V1 _V6
V1 _V4
V4 _V6
V1_V6, lead1,aVL
lead1,aVL,V5,V6
lead1 , aVL
lead2,lead 3,avf
ST depression &
prominent R in
V1 -V4
Anterior MI
Anteroseptal MI
Anterolateral MI
Extensive anterior
MI
Lateral MI
high lateral MI
inferior MI
posterior MI
LAD
LAD
LMCA
LCX
RCA
RCX
Sites
LAD
LCX

78. What are The reciprocal changes?
Reciprocal ST-segment depression, also known as
reciprocal change, is defined as ST - segment
depression in leads separate and distinct from leads
that reflect ST -segment elevation .
Reciprocal change is seen in approximately 75% of
patients with inferior wall MI and frequently in
lateral STEMI.
Reciprocal change is an important ECG concept to
consider for two reasons. First, it identifies patients
with a high-risk ACS presentation & Second , the
presence of reciprocal change is strong confirmatory
evidence that STEMI is present.

79. Examples on reciprocal changes :
Reciprocal changes
(ST depression)
Type of MI
In lead 1 & aVLInferior MI
Lateral MI In lead2,lead3 & aVF

80. Anterior wall MI

81. Another example on
Anterior wall MI

82. Anterior wall MI
There are hyperacute T-waves in V2-6 (most
marked in V2 and V3) with loss of R wave
height.

83. Anteroseptal MI

84. Another example on
Anteroseptal MI

85. Extensive anterior MI

86. Another example on
Extensive anterior MI

87. Lateral MI
There is reciprocal ST depression in the
inferior leads (III and aVF)

88. Another example on
lateral MI

89. Inferior MI
There is ST elevation in II, III and aVF with
Reciprocal ST depression and T wave
inversion in aVL

90. Important note :
Up to 40% of patients with an inferior STEMI will have a
concomitant right ventricular infarction.
These patients may develop severe hypotension in
response to nitrates and generally have a worse
prognosis.
If the ST elevation in lead III > II with reciprocal change
present in lead I ± aVL , It may suggests an associated RV
infarction. This patient should have right-sided leads to
confirm this.
After we did the right sided ECG , if the ST elevation
is persist especially in V4 , the patient have right
ventricular infarction .

91. Another example
There is ST elevation in II, III and aVF with
Reciprocal ST depression.
ST elevation in lead III > I

92. Posterior MI
* It usually occur in the context of an inferior or lateral
infarction.
*Isolated posterior MI is less common.
*Explanation of the ECG changes in V1-4:
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

93. Isolated posterior MI
ST depression in V2-4
Tall, broad R waves in V2-3

94. Inferolateral MI , 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

95. ST depression (leads I, II, V5-6) it could be
Unstable angina or NSTEMI.
We differentiate between them by the cardiac
enzymes .

96.  ABC
 Measure the vital signs
 Put the patient on a monitor
 Give O2 if there is low oxygen saturation
 Aspirin 300 mg chewable
 Plavix 300 mg
 Nitroglycerin, unless hypotensive (sublingual 300 _ 500 mg)
 Heparin
 Morphine (2.5 _10mg) & give metoclopramide (10mg)
 Beta Blocker
Then
choose
Either OR
PCI
Which is the best
RX but it should
be given within 2
hours
Thrombolytic
therapy
According to the
indication & the
absence of C.I

97. Indication of thrombolytic therapy :
1 : ischemic chest pain ˂ 12 hour
2 : ECG changes :
A : ST elevation ˃ 1 mm in 2 contagious
limb lead
B : ST elevation ˃ 2 mm in 2 contagious
chest lead
C : new or presumed new LBBB
D : posterior MI

98. Some of the contraindication of
thrombolytic therapy :
Absolute Relative
 Previous hemorrhagic
stroke at any time
 Previous ischemic stroke
within the past 1 year
 Suspected aortic
dissection
 Known intracranial
neoplasm
 Previous allergic reaction
to fibrinolytic agent
 Uncontrolled
hypertension
 Recent surgery (within 1
month)
 Pregnancy
 High probability of active
peptic ulcer
 Previous subarachnoid or
intracerebral
hemorrhage

99. 7Other
Cases

100. Pericarditis
ECG characteristics :
* ST elevation with upward concavity
* PR interval depression which is a more
specific indicator
Some refer to the concave upwards ST elevation as the "smily face" of
pericarditis compared with the “sad face" of STEMI.

101. Widespread concave ST elevation and PR
depression is present throughout the precordial
(V2-6) and limb leads (I, II, aVL, aVF).

102. Hyperkalemia
The following ECG changes listed
sequentially as K level increase :
• Tall , symmetrically peaked T wave
• ST depression
• P-R prolongation , widening and flattening
of P wave
• P wave disappearances
• QRS widening and fusion with tall T wave
• Ventricular tachycardia , ventricular flutter ,
ventricular fibrillation , ventricular standstill

103. Early ECG changes
showing Peaked T waves

104. Prolonged PR interval
Broad, bizarre QRS complexes
Peaked T waves

105. Hypokalemia
ECG characteristics :
• Lowering and inversion of T wave
• Prominent U wave
• ST depression
• Prominent P wave and prolongation of
PR interval
• Atrial & ventricular arrhythmias including
ventricular tachycardia & ventricular
fibrillation

106. ST depression.
T wave inversion.
Prominent U waves

107. Pulmonary Embolism
The ECG may offer some help when assessing
patients who are suspected of having PE :
• ECG may be normal
• Sinus tachycardia , and other transient
supraventricular arrhythmias such as atrial
fibrillation , atrial flutter .
• P Pulmonale
• RBBB
• ST depression & T wave inversion in the V1 & V2
• RAD
• S1 Q3 T3 ( S wave in lead 1 , Q wave in lead 3 ,
inverted T wave in lead 3 )

108. RBBB
RAD
S1 Q3 T3
T-wave inversions in V1 V2

109. Quizzes

110. Case 1 : 35 year old patient admitted to ICU because of
palpitation & SOB of 1 day duration , he had occasional such attacks
since 1 year. He has no history of hypertension or DM. Physical
examination revealed rapid heart rate , BP 125/85mmHg with
mid diastolic murmur in mitral area.
ECG showed the following changes :

111. Q1 : What are the ECG changes ?
Q2 : What is the diagnosis ?
Q3 : How you will manage this case ?

112. The answer is Atrial
Fibrillation

113. Case 2 : 57 year old patient presented with palpitation ,
SOB & dizziness . Physical examination revealed rapid heart
rate , BP 130/70mmHg.
ECG showed the following changes :

114. Q1 : What are the ECG changes ?
Q2 : What is the diagnosis ?
Q3 : How you will manage this case ?

115. The answer is
SVT

116. Case 3 : 60 year old patient admitted to ICU because of
severe retrosternal chest pain persisting more than 30
minutes with vomiting & profuse sweating.
ECG showed the following changes :

117. Q1 : What are the ECG changes ?
Q2 : What is the diagnosis ?
Q3 : How you will manage this case
?

118. The answer is
extensive anterior
MI

119. Case 4 : 70 year old patient presented with
fatigue , dizziness & impaired exercise tolerance .
He is on digoxin treatment.
ECG showed the following changes :

120. Q1 : What are the ECG changes ?
Q2 : What is the diagnosis ?
Q3 : How you will manage this case ?
Q4 : mention 3 causes

121. The answer is
third degree
heart block

122. Case 5 : 70 year old patient presented with retrosternal
chest pain , then he developed hypotension , bradycardia &
↑ JVP , the chest was clear with no tachyarrhythmia .
ECG showed the following changes :

123. Q1 : What are the ECG changes ?
Q2 : What is the diagnosis ?
Q3 : what is the complication in this
case ? How to confirm it ?
Q4 : How you will manage
this case ?

124. The answers are :
* Dx : Inferior MI
* Complication : RV infarction & we confirm it
by right sided ECG
* Rx : the same RX of STEMI
but without nitroglycerine

125. Case 6 : 45 year old patient presented to the ED
with retrosternal chest pain , radiating to lower jaw
of 20 minutes duration.
ECG showed the following changes :

126. Q1 : What are the ECG changes ?
Q2 : Give 2 differential diagnosis ?
Q3 : how to differentiate between
them ?
Q4 : How you will
manage this case ?

127. The answer :
The ECG shows ST depressions , so the
diagnosis will be either NSTEMI or UNSTABLE
ANGINA , the cardiac enzymes will
differentiate between them .

128. References:
1: Davidson's principles and practice of medicine, 22nd edition
2: The ECG made easy, seventh edition
3: ACLS guidelines 2015
4: ECG for medical students and general practitioners, 1st edition
5: Learn ECG in a day, 1st edition
6: ECG notes interpretation and management guide, 1st edition
7: www.medscape.com
www.lifeinthefastlane.com
www.ecgpedia.org