1. Santhiram Medical College
Nandyal
ELECTROCARDIOGRAPHY
Lecture By
Dr.G.Venkata Swamy M.D

2. HISTORY OF
ELECTROCARDIOPHY
 Agustus – Desire’ Waller was the first
person to record cardiac electricity in 1887
 But most comprehensive work on human
electrocardiography was done by Willem
Einthoven in 1903
 Willem Einthoven was awarded Nobel
prize for his work in electrocardiography in
1924
 A few years later Wilson and Goldberger
developed the unipolar and augmented
unipolar systems respectively

3. Definitions
Electrocardiogram (ECG) :
It is a graphic recording of electric
potentials generated by the heart.
Electrocardiography :
The process of recording ECG
is called electrocardiography
Electrocardiograph :
The machine that records the ECG
is called electrocardiograph
Lead : Electrode placed on the body is
called a lead

4. Ctn. Electrocardiogram (ECG)
• An ECG is a series of waves and deflections recording the
heart’s electrical activity from a certain “view.” Many views,
each called a lead, monitor voltage changes between electrodes
placed in different positions on the body.
• Leads I, II, and III are bipolar leads, which consist of two
electrodes of opposite polarity (positive and negative). The third
(ground) electrode minimizes electrical activity from other
sources.
• Leads aVR, aVL, and aVF are unipolar leads and consist of a
single positive electrode and a reference point (with zero
electrical potential) that lies in the center of the heart’s
electrical field.
• Leads V1–V6 are unipolar leads and consist of a single positive
electrode with a negative reference point found at the electrical
center of the heart.

5. Clinical utility of the ECG :
1. It is noninvasive inexpensive and
highly versatile test
2. Useful in detecting
a) Arrhythmias
b) Conduction disturbances
c) myocardial ischemia & infarction
and
d) metabolic disturbances such as
Hyperkalemia and Hypokalemia

6. Electrocardiogram
1. Basics
2. Axis determination
3. Calculation of Heart Rate
4. Arrhythmias
5. Bundle Branch Blocks
6. Myocardial infarction
7. Cardiac enlargement and
Hypertrophy
8. AV Blocks

7. Ctn. Structure and Function of the Normal Heart and Blood Vessels

8. Conduction System
sinoatrial node
located in right atrium inf. to
opening of SVC
action potential begins here
initiates atrial contraction
atrioventricular node
located in right atrium ant. to
opening of coronary sinus
main job is to delay the action
potential to give atria time to
contract
bundle of His (AV bundle)
only site where atrial impulses can
travel to the ventricles
bundle branches
Purkinje fibers (not shown)
small branches that travel from
endocardium into myocadium

9. Conduction System
Review
cardiac action potential is initated in
the SA node
travels quickly through pathways to
simultaneously contract the atria
the atria and ventricles are insulated
from each other so atrial action
potentials can only enter ventricles
through one pathway
action potential enters AV node where
the impulses are slowed down and
held momentarily
this gives the atria time to contract
the action potential then travels
quickly to the rest of the ventricular
myocardium through the AV bundle,
bundle branches and purkinje fibers

10. Electrical Flow
resting myocardial cells have a net negative
charge at rest
when an AP reaches a cell it depolarizes
causing the internal net charge to become
positive
electrically, the action potential traveling
through the heart can be viewed as a wave
of positive charge
Vector
the average direction of all of the positive
charges as they travel through the
myocardium
the average vector in a normal heart
travels to the left and downward

11. Electrical Flow
Vector Influences
things that influence the
overall amount of charge
flowing through the
myocardium will change the
average direction the the
charge is flowing
Infarction
essentially an area that no
longer carries charge
what would happen to the
vector if the posterior wall of
the l. ventricle infarcted?

12. Electrical Flow
Vector Influences
things that influence the overall
amount of charge flowing through the
myocardium will change the average
direction the the charge is flowing
Infarction
essentially an area that no longer carries
charge
what would happen to the vector if the
posterior wall of the l. ventricle infarcted?
Hypertrophy
essentially an area that carries extra
charge
how would the vector change with l.
ventricular hypertrophy?
vector points towards hypertrophy and
away from infarction

13. ECG PAPER
• The horizontal scale represents time,
such that, at a standard paper speed
of 25 mm/sec, each small box (1 mm)
represents 0.04 second and each large
box (5 mm) represents 0.20 second.
• The vertical scale represents amplitude
(10 mm = 1 mV). The heart rate can be
estimated by dividing the number of
large boxes between complexes (R-R
interval) into 300.

14. ECG graph paper

15. Ctn. Electrocardiogram (ECG)

16. Ctn. Electrocardiogram (ECG)

17.  In the ECG each wave has a height
(positive deflection )
or depth (negative deflection and
width)
 When current flows towards
an electrode a tall positive deflection
is recorded
 When current flows away from the
electrode a deep negative deflection
is recorded
 When current flows at 900 to
the electrode a small ½ positive and

18.  When current flows towards
an electrode a tall positive deflection
is recorded fig. – E1 electrode

19.  When current flows away from the
electrode a deep negative deflection
is recorded fig – E2 electrode

20.  When current flows at 900 to
the electrode a small ½ positive and
½ negative deflections are recorded
fig – E3 electrode

22. Ctn. Electrocardiogram (ECG)

23. Ctn. Electrocardiogram (ECG)

24. Standard Limb Leads

25. Ctn. Electrocardiogram (ECG)
Standard Limb Electrode Placement
Standard Limb Leads

26. Standard Limb Leads

27. Ctn. Electrocardiogram (ECG)
Standard Limb Electrode Placement
Augmented Limb Leads

28. Augmented Limb Leads

29. All Limb Leads

31. Ctn. Electrocardiogram (ECG)
Standard Chest Lead Electrode Placement
The Right-Sided 12-Lead ECG The 15-Lead ECG

32. ECG AXIS DETERMINATION

33. Direction of LEAD – 1 LEAD-2
AXIS
QRS compels DOMINANTLY DOMINANTY
NORMAL
POSITIVE POSITIVE

34. DIRECTION LEAD – 1 LEAD – 2
AXIS
OF QRS DOMINANTLY DOMINANTLY LAD
COMPLEX POSITIVE NEGATIVE
1. NORMAL VARANT 2. LVH
3. LEFT ANTERIOR FASCICULAR BLOCK
4. INFERIOR M I

35. DIRECTION LEAD1 LEAD2
AXIS
OF QRS DOMINANTLY DOMINANTLY
RAD
COMPLEX NEGATIVE POSITIVE
1. NORMAL VARIENT 2. DEXTROCARDIA
3. SPURIOUS FINDING DUE TO REVERSAL OF
RIGHT AND LEFT ARM ELECTRODES

36. AXIS DETERMINATION
 TO DETERMINE THE AXIS, LOCATE THE FRONTAL PLANE
LEAD WHICH SHOWS SMALL EQUIPHASIC QRS DEFLETION
 ITS PERPENDICULAR LEAD FORMS THE ELECTRICAL AXIS
OF THEHEART WHICH SHOWS MAXIMUM QRS DEFLECTION
 IF THE DEFLECTION IS POSITIVE THE AXIS IS THE AXIS
OF THE POSITIVE POLE OF THAT LEAD
 IF THE DEFLECTION IS NEGATIVE THE AXIS IS THE AXIS
OF THE NEGATIVE POLE OF THAT LEAD

37. In this figure small equiphasic QRS
deflection is AVR THE LEAD WHICH
IS AT 90O IS LIII. IN LIII THE
DEFLECTION IS POSTIVE SO THE
AXIS IS +1200

38. IN THIS FIGUER SMALL EQUIPHASIC
QRS DEFLECTION IS LII. THE LEAD AT
900 TO LII LEAD IS AVL . IN THIS LEAD
THE DEFLECTION IS NEGATIVE SO
THE AXIS IS +1500

40. Ctn. Electrocardiogram (ECG)
 Methods for Calculating Heart Rate
• Method 1: Count Large Boxes: Regular rhythms
can be quickly determined by counting the number of large
graph boxes between two R waves. That number is divided
into 300 to calculate bpm.

41. Ctn. Electrocardiogram (ECG)
• Method 2: Count Small Boxes: Sometimes it is
necessary to count the number of small boxes
between two R waves for fast heart rates. That
number is divided into 1500 to calculate bpm.

42. Ctn. Electrocardiogram (ECG)
• Method 3: Six-Second ECG Rhythm
Strip: The best method for measuring
irregular rates with varying R-R intervals is
to count the
• number of R waves in a 6-sec strip and
multiply by 10. This gives the average
number of bpm.

43. Ctn. Electrocardiogram (ECG)

45. Electrocardiogram
Arrhythmias

46. Normal Sinus Rhythm
(NSR)
Rate: Normal (60–100 bpm)
Rhythm: Regular
P Waves: Normal (upright and uniform)
PR Interval: Normal (0.12–0.20 sec)
QRS: Normal (0.06–0.10 sec)

47. Asystole
Rate: None
Rhythm: None
P Waves: None
PR Interval: None
QRS: None

48. Sinus Bradycardia
Rate: Slow (<60 bpm)
Rhythm: Regular
P Waves: Normal (upright and
uniform)
PR Interval: Normal (0.12–0.20
sec)
QRS: Normal (0.06–0.10 sec)

49. Sinus Tachycardia
Rate: Fast (>100 bpm)
Rhythm: Regular
P Waves: Normal (upright and
uniform)
PR Interval: Normal (0.12–0.20
sec)
QRS: Normal (0.06–0.10 sec)

50. Sinus Arrhythmia
Rate: Usually normal (60–100 bpm);
frequently increases with inspiration
and decreases with expiration
Rhythm: Irregular; varies with respiration
P Waves: Normal (upright and uniform)
PR Interval: Normal (0.12–0.20 sec)
QRS: Normal (0.06–0.10 sec)

51. Sinus Pause (Sinus Arrest)
Rate: Normal to slow; determined by
duration and frequency of sinus pause
Rhythm: Irregular whenever a pause (arrest)
occurs
P Waves: Normal (upright and uniform)
except in areas of pause (arrest)
PR Interval: Normal (0.12–0.20 sec)
QRS: Normal (0.06–0.10 sec)

52. Sinoatrial (SA) Block
Rate: Normal to slow; determined by duration and frequency
of SA block
Rhythm: Irregular whenever an SA block occurs
P Waves: Normal (upright and uniform) except in areas of
dropped beats
PR Interval: Normal (0.12–0.20 sec)
QRS: Normal (0.06–0.10 sec)
• The block occurs in some multiple of the P-P interval.
• After the dropped beat, cycles continue on time.

53. Supraventricular Tachycardia (SVT)
Rate: 150–250 bpm
Rhythm: Regular
P Waves: Frequently buried in preceding T waves and
difficult to see
PR Interval: Usually not possible to measure
QRS: Normal (0.06–0.10 sec) but may be wide if
abnormally conducted through ventricles
• This arrhythmia has such a fast rate that the P
waves may not be seen.

54. Atrial Flutter (A-flutter)
Rate: Atrial: 250–350 bpm; ventricular: slow or fast
Rhythm: Usually regular but may be variable
P Waves: Flutter waves have a saw-toothed
appearance
PR Interval: Variable
QRS: Usually normal (0.06–0.10 sec), but may
appear widened if flutter waves are buried in QRS

55. Atrial Fibrillation (A-fib)
Rate: Atrial: 350 bpm or greater; ventricular: slow or
fast
Rhythm: Irregular
P Waves: No true P waves; chaotic atrial activity
PR Interval: None
QRS: Normal (0.06–0.10 sec)
• Rapid, erratic electrical discharge comes from
multiple atrial ectopic foci.
• No organized atrial contractions are detectable.

56. Ctn. Electrocardiogram (ECG)
Premature Ventricular Contraction (PVC)
Ventricular Tachycardia (VT)

57. Ctn. Electrocardiogram (ECG)
Torsade de Pointes
Ventricular Fibrillation (VF)

58. Myocardial infarction

60. The 12-Lead ECG
 The 12-Lead ECG sees the heart
from 12 different views.
 Therefore, the 12-Lead ECG
helps you see what is happening
in different portions of the
heart.
 The rhythm strip is only 1 of
these 12 views.

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

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

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

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

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

67. 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.

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

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

70. Other MI Locations
Now that you know where to look for
an anterior wall myocardial infarction
let’s look at how you would determine
if the MI involves the lateral wall or
the inferior wall of the heart.

71. Other MI Locations
First, take a Lateral portion
look again at of the heart
this picture of
the heart.
Anterior portion
of the heart
Inferior portion
of the heart

72. 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

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

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

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

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

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

78. Putting it all Together
How about now?

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

80. Right Ventricular Infarction
 R.V infarction is associated with
inferoposterior infarcation
 RV infarcation causes signs of sever RV
failure
( JVP , Kussmaul’s sign , tender
hepatomegaly with or without hypotension )
 ST segment elevation is present in
V1 V2 and V4 R

81. Bundle branch blocks

82. Left Bundle Branch Block
Criteria
 QRS duration ≥ 120ms
 Broad R wave in I and V6
 Prominent QS wave in V1
 Absence of q waves (including
physiologic q waves) in I and V6

83. Right Bundle Branch Block
Criteria
 QRS duration ≥ 110ms
 rSR’ pattern or notched R wave in V1
 Wide S wave in I and V6

84. Chamber Enlargement And
Hypertrophy

85. Left Atrial Enlargement
Criteria
P wave duration in II ≥120ms
or
Negative component of
biphasic P wave in V1 ≥ 1 “small
box” in area

86. Right Atrial Enlargement
Criteria
P wave height in II ≥ 2.4mm
or
Positive component of
biphasic P wave in V1 ≥ 1
“small box” in area

87. Left Ventricular Hypertrophy
Many sets of criteria for diagnosing LVH
have been proposed:
Sensitivity Specificity
The sum of the S wave in V1
and the R wave in either V5 43% 95%
or V6 > 35 mm
Sum of the largest precordial
R wave and the largest 45% 93%
precordial S wave > 45 mm
Romhilt-Estes Point System 50-54% 95-97%

88. Left Ventricular Hypertrophy

89. Right Ventricular Hypertrophy
 Right axis deviation
 Right atrial enlargement
 Downsloping ST depressions in V1-V3 (a.k.a.
RV strain pattern)
 Tall R wave in V1

90. Right Ventricular Hypertrophy

91. Examples

92. Left Ventricular Hypertrophy

93. Right Bundle Branch Block

94. Right Atrial Enlargement

95. Left Bundle Branch Block

96. Left Atrial Enlargement

97. Right Ventricular Hypertrophy

98. Left Ventricular Hypertrophy
(with frequent PVCs)

99. A-V BLOCKS
 Interruption/delay in the conduction
of electrical impulses between the
atria & ventricles
 Classified site of block/severity of
conduction abnormality
 1st degree, 2nd degree Mobitz I
(Wenkebach), 2nd degree Mobitz II, 3rd
degree (Complete heart block)

100. 1 Degree AV Block
st
 Characterized by PR Interval > 0.20
seconds
 Delay in conduction AV Node
 Prolonged PR Interval constant
 Usually asymptomatic
 Least concerning of the blocks

101. 2nd Degree Mobitz I
(Wenkebach)
 Successive impulses from SA node delayed
slightly longer than the previous impulse
 Characterized by prolonged PR interval that
continues until the P wave is dropped (impulse
doesn’t reach ventricle)
 May have hypotension or lightheadedness

102. 2 Degree Mobitz II
nd
 Less common, more serious
 Impulses from SA node fail to conduct to
ventricles
 Hallmark PR Interval constant normal or
prolonged, doesn’t prolong before dropping, not
followed by QRS, can have > 1 dropped in a row
 Precursor to 3rd Degree Heart Block

104. 3RD DEGREE “COMPLETE
HEART BLOCK”
 Indicates complete absence of impulse between
the atria & ventricle
 Atrial rate > or = ventricular rate
 Occur @ AV node 40-60 bpm
 Occur @ bundle branches < 40 bpm wide QRS
complex
 Decreased C.O., P-P & R-R disassociated

105. Hypokalemia
 Clinical consequences of hypokalemia
usually goes unnoticed. Common
findings include weakness, fatigue,
constipation, ileus, and respiratory
muscle dysfunction.
 Thus, most of the time K+ gets
replaced out of habit or to please the
consultants. (e.g. Cardiology likes a
K+ of 4.0 or above in MI patients.)

106. Don’t Forget about EKG
 ST depressions with prominent U waves and prolonged
repolarization

107. Definition
 Normal serum potassium 3.5-5.5
mEq/L
 Hyperkalemia is a serum
potassium greater than 5.5
mEq/L

108. EKG Changes
Peaked T Waves