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.
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 .
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
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
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
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
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
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
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).
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
V1V6 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 .