The document discusses the history and development of electrocardiography (ECG/EKG) and summarizes the key aspects of ECG interpretation. Some of the main points covered include: - The key individuals who contributed to the development of ECG, from its initial discovery in the 1800s to modern applications. - The components of a standard 12-lead ECG, including the waves, intervals, leads, and their normal values and appearances. - Common ECG abnormalities such as arrhythmias, conduction blocks, hypertrophy, ischemia, and injury patterns. - Guidelines for proper ECG acquisition and systematic interpretation.

1. Presented by
Aser mohamed kamal

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

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

6. An electrocardiogram (EKG or ECG) is a
test that checks for problems with the
electrical activity of your heart. An EKG
translates the heart's electrical activity into
line tracings on paper. The spikes and dips
in the line tracings are called waves. The
heart is a muscular pump made up of four
chambers .

7. Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers

8. X- Axis time in seconds
Y-AxisAmplitudeinmillvolts

9.  X-Axis represents time - Scale X-Axis – 1 mm = 0.04 sec
 Y-Axis represents voltage - Scale Y-Axis – 1 mm = 0.1 mV
 One big square on X-Axis = 0.2 sec (big box)
 Two big squares on Y-Axis = 1 milli volt (mV)
 Each small square is 0.04 sec (1 mm in size)
 Each big square on the ECG represents 5 small squares
= 0.04 x 5 = 0.2 seconds
 5 such big squares = 0.2 x 5 = 1sec = 25 mm
 One second is 25 mm or 5 big squares
 One minute is 5 x 60 = 300 big squares

10. P wave
PR Interval
QRS complex
ST segment
T Wave
QT Interval
RR Interval

11.  P Wave is Atrial contraction – Normal 0.12
sec
 PR interval is from the beginning of P wave to
the beginning of QRS – Normal up to 0.2 sec
 QRS is Ventricular contraction –Normal 0.08
sec
 ST segment – Normal Isoelectic (electric
silence)
 QT Interval – From the beginning of QRS to
the end of T wave – Normal – 0.40 sec
 RR Interval – One Cardiac cycle 0.80 sec

13. # of
Boxes
DurationThe Wave or Interval
(3)0.12 secP wave : Atrial contraction
(5)0.20 secPR interval – P to begin. of QRS
(2)0.08 secQRS complex - Ventricular
IsoelectricST segment - Electrical silence
(3)0.12 secT wave - repolarization
(2)0.08 secQRS interval – Ventricular cont.
(10)0.40 secQT interval - From Q to T end
(5)0.20 secTP segment - Electrical silence

14. 1
2
3
4
5
6
7
8

15. 1. P wave – Atrial contraction = 0.12 sec (3 small
boxes)
2. PR Interval – P + AV delay = 0.20 sec (5 small
boxes)
3. Q wave – Septal = < 3 mm, < 0.04 sec (1 small
box)
4. R wave – Ventricular contraction < 15 mm
5. S wave – complimentary to R < 15 mm
6. ST segment – Isoelectric – decides our fate
7. T wave – ventricular repolarization – friend of ST
8. TP segment – ventricular relaxation – shortened
in tachycardia

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

17. +
+ +
- - -
R L
F
R
F
L

18. Standard ECG is recorded in 12 leads
Six Limb leads – L1, L2, L3, aVR, aVL,
aVF
Six Chest Leads – V1 V2 V3 V4 V5 and V6
L1, L2 and L3 are called bipolar leads
L1 between LA and RA
L2 between LF and RA
L3 between LF and LA

19. ++
+
Lead aVR Lead aVL Lead aVF
R L
F

20. Standard ECG is recorded in 12 leads
Six Limb leads – L1, L2, L3, aVR, aVL,
aVF
Six Chest Leads – V1 V2 V3 V4 V5 and V6
 aVR, aVL, aVF are called unipolar leads
aVR – from Right Arm Positive
aVL – from Left Arm Positive
aVF – from Left Foot Positive

21. The standard EKG has 12 leads:
3 Standard Limb Leads
3 Augmented Limb Leads
6 Precordial Leads

29. Precardial (chest) Lead Position
V1 Fourth ICS, right sternal border
V2 Fourth ICS, left sternal border
V3 Equidistant between V2 and V4
V4 Fifth ICS, left Mid clavicular Line
V5 Fifth ICS Left anterior axillary line
V6 Fifth ICS Left mid axillary line

36. Professor Chamberlains 10 rules of
normal:-

37.  PR interval should be 120 to 200
milliseconds or 3 to 5 little squares

38. The width of the QRS complex should
not exceed 110 ms, less than 3 little
squares

39. The QRS complex should be
dominantly upright in leads I and II

40. QRS and T waves tend to have the same
general direction in the limb leads

41. All waves are negative in lead aVR

42.  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

43. The ST segment should start isoelectric
except in V1 and V2 where it may be
elevated

44.  The P waves should be upright in I, II, and V2
to V6

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

46. The T wave must be upright in I, II, V2 to
V6

47.  Correct Lead placement and good contact
 Proper earth connection, avoid other gadgets
 Deep inspiration record of L3, aVF
 Compare serial ECGs if available
 Relate the changes to Age, Sex, Clinical
history
 Consider the co-morbidities that may effect
ECG
 Make a xerox copy of the record for future
use
 Interpret systematically to avoid errors

49.  Standardization – 10 mm (2 boxes) = 1 mV
 Double and half standardization if required
 Sinus Rhythm – Each P followed by QRS, R-R
constant
 P waves – always examine for in L2, V1, L1
 QRS positive in L1, L2, L3, aVF and aVL. – Neg in
aVR
 QRS is < 0.08 narrow, Q in V5, V6 < 0.04, < 3 mm
 R wave progression from V1 to V6, QT interval <
0.4
 Axis normal – L1, L3, and aVF all will be positive
 ST Isoelectric, T waves ↑, Normal T↓ in aVR,V1,
V2

50.  Normal Resting ECG – cannot exclude disease
 Ischemia may be covert – supply / demand equation
 Changes of MI take some time to develop in ECG
 Mild Ventricular hypertrophy - not detectable in ECG
 Some of the ECG abnormalities are non specific
 Single ECG cannot give progress – Need serial
ECGs
 ECG changes not always correlate with Angio
results
 Paroxysmal events will be missed in single ECG

51.  May have slight left axis due to rotation of
heart
 May have high voltage QRS – simulating LVH
 Mild slurring of QRS but duration < 0.09
 J point depression, early repolarization
 T inversions in V2, V3 and V4 – Juvenile T ↓
 Similarly in women also T↓
 Low voltages in obese women and men
 Non cardiac causes of ECG changes may
occur

52. Always positive in lead I and II
Always negative in lead aVR
< 3 small squares in duration
< 2.5 small squares in amplitude
Commonly biphasic in lead V1
Best seen in leads II

53. -Tall (> 2.5 mm), pointed P waves (P Pulmonale)

54. Notched/bifid (‘M’ shaped) P wave (P
‘mitrale’) in limb leads

55. P Pulmonale
P Mitrale

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

57. First degree Heart Block

58.  Nonpathological Q waves may present in I,
III, aVL, V5, and V6
 R wave in lead V6 is smaller than V5
 Depth of the S wave, should not exceed 30
mm
 Pathological Q wave > 2mm deep and > 1mm
wide or > 25% amplitude of the subsequent R
wave

60.  Sokolow & Lyon
Criteria
 S in V1+ R in V5 or
V6 > 35 mm
 An R wave of 11 to 13
mm (1.1 to 1.3 mV) or
more in lead aVL is
another sign of LVH

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

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

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

67. Rule of 300/1500
10 Second Rule

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

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

70. (300 / 6) = 50 bpm

71. (300 / ~ 4) = ~ 75 bpm

72. 33 x 6 = 198 bpm

73. (300 / 1.5) = 200 bpm

78.  Is a Coronary artery disease is most commonly caused by
obstructive atherosclerosis of epicardial coronary arteries.
This leads to an inadequate perfusion of the myocardium and
causes an imbalance between myocardial tissue oxygen
supply and demand (myocardial ischemia).
 Ischaemic (or ischemic) heart disease is a disease
characterized by reduced blood supply to the heart.
 It is the most common cause of death in most western
countries.
 Ischaemia means a "reduced blood supply".
 The coronary arteries supply blood to the heart muscle and no
alternative blood supply exists, so a blockage in the coronary
arteries reduces the supply of blood to heart muscle.

79.  Most ischaemic heart disease is caused by atherosclerosis,
usually present even when the artery lumens appear normal
by angiography.
 Initially there is sudden severe narrowing or closure of either
the large coronary arteries and/or of coronary artery end
branches by debris showering downstream in the flowing
blood.
 It is usually felt as angina, especially if a large area is affected.
 The narrowing or closure is predominantly caused by the
covering of atheromatous plaques within the wall of the artery
rupturing, in turn leading to a heart attack (Heart attacks
caused by just artery narrowing are rare).
 A heart attack causes damage to heart muscle by cutting off
its blood supply.

80. 1.Poor R wave progression :
Loss of gradual progression (increase) in
amplitude of R waves in chest leads from
V1V6 if this gradual increase is lost this
is sign of IHD .
2.Q waves:
Presence of deep Q waves in related
leads (inferior , antoroseptal and lateral )
donates old MI.

81. 3. T wave inversion in related leads MAY
BE a sign of IHD . Other causes :
- LVH
- stroke
-pericardaities
-normal in V1,V2 (in female)

82. 4. ST segment :
Elevation :-
- acute MI .
- acute percardities .
-early repolarization pattern in young age
Depression :-
-horizontal depression  IHD(angina).
-down sloping depression  IHD(angina).

83. 5. Lost of R wave progression :
Ischemic cardiomyopathy .

84. 1.LA:
a) Wide P wave in limb leads .
b) Biphasic P wave in V1: -ve component
deeper than +ve component .
2.LV:
a) R amplitude in aVL >13mm.
b) Tallest R wave + deepest >35mm .
c) R wave or S wave > 25mm .

85. 3. RA:
tall peaked P wave in limb leads.
4. RV:
tall R waves in V1 , V2 .