2. Dr Awadhesh Kr Sharma
Dr. Awadhesh kumar sharma is a young, diligent and dynamic interventional cardiologist. He did his
graduation from GSVM Medical College Kanpur and MD in Internal Medicine from MLB Medical college
jhansi. Then he did his superspecilisation degree DM in Cardiology from PGIMER & DR Ram Manoher
Lohia Hospital Delhi. He had excellent academic record with Gold medal in MBBS,MD and first class in
DM.He was also awarded chief ministers medal in 2009 for his academic excellence by former chief
minister of UP Smt Mayawati in 2009.He is also receiver of GEMS international award.He had many
national & international publications.He is also in editorial board of international journal- Journal of clinical
medicine & research(JCMR).He is also active member of reviewer board of many journals.He is also trainee
fellow of American college of cardiology. He is currently working in NABH Approved Gracian
Superspeciality Hospital Mohali as Consultant Cardiologist.
3. The goal of this academic session is-
To have basic understanding of ECG waves &
intervals.
Interpretation of ECG
Outline the criteria for the most common
electrocardiographic diagnoses in adults.
Describe critical aspects of the clinical application of
the ECG
4. HISTORY
1842- Italian scientist Carlo Matteucci realizes that electricity
is associated with the heart beat.
1895 - William Einthoven , credited for the invention of ECG.
1906 - using the string electrometer ECG,William Einthoven
diagnoses some heart problems.
1924 - The noble prize for physiology or medicine is given to
William Einthoven for his work on ECG
5.
6. ELECTROCARDIOGRAM
The electrocardiogram (ECG) is a
representation of the electrical events of the
cardiac cycle.
Each event has a distinctive waveform, the
study of waveform can lead to greater insight
into a patient’s cardiac patho physiology.
7. ECGs can identify
Arrhythmias
Myocardial ischemia and infarction
Pericarditis
Chamber hypertrophy
Electrolyte disturbances (i.e. hyperkalemia,
hypokalemia)
Drug toxicity (i.e. digoxin and drugs which
prolong the QT interval)
8. Recent advances have extended the importance
of the ECG.
It is a vital test for determining -
1. The presence and severity of acute myocardial
ischemia/infarction.
2. Localizing sites of origin and pathways of tachyarrhythmias,
3. Assessing therapeutic options for patients with heart failure,
4. Identifying and evaluating patients with genetic diseases who
are prone to arrhythmias.
9. Fundamental Principles
Transmembrane ionic currents are generated by ion fluxes
across cell membranes and between adjacent cells.
These currents are synchronized by cardiac activation and
recovery sequences to generate a cardiac electrical field in
and around the heart that varies with time during the
cardiac cycle.
The currents reaching the skin are then detected by
electrodes placed in specific locations on the extremities
and torso that are configured to produce leads.
10. Fundamental Principles
Transmembrane ionic currents are ultimately responsible
for the potentials that are recorded as an ECG.
Electrophysiological currents are considered to be the
movement of positive charge.
An electrode senses positive potentials when an activation
front is moving toward it and negative potentials when the
activation front is moving away from it.
11. Depolarization
Contraction of any muscle is associated with
electrical changes called depolarization.
These changes can be detected by electrodes
attached to the surface of the body.
12. Repolarization
Phase of recovery/relaxation.
The dipole moment at any one instant during recovery is
less than during activation.
Recovery, is a slow process, lasts 100 msec or longer and
occurs simultaneously over extensive portions of the fiber.
13. Pacemakers of the Heart
SA Node - Dominant pacemaker with an intrinsic rate of 60 -
100 beats/minute.
AV Node - Back-up pacemaker with an intrinsic rate of 40 - 60
beats/minute.
Ventricular cells - Back-up pacemaker with an intrinsic rate of
20 - 45 bpm.
17. ECG Leads
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. ECG Leads
The standard ECG has 12 leads:
3 Standard Limb Leads
3 Augmented Limb Leads
6 Precordial Leads
19. Recording of the ECG
Limb leads are I, II, II.
Each of the leads are bipolar; i.e., it requires two sensors on
the skin to make a lead.
If one connects a line between two sensors, one has a vector.
There will be a positive end at one electrode and negative at
the other.
The positioning for leads I, II, and III were first given by
Einthoven (Einthoven’s triangle).
26. The ECG Paper
Horizontally
One small box - 0.04 s
One large box - 0.20 s
Vertically
One large box - 0.5 mV
27. Clinical Interpretation of the ECG
Accurate analysis of ECGs requires thoroughness and
care.
The patient's age, gender, and clinical status should
always be taken into account.
Many mistakes in ECG interpretation are errors of
omission. Therefore, a systematic approach is
essential.
30. The following 14 points should be analyzed carefully in every
ECG:
1. Standardization (calibration) and technical features (including lead
placement and artifacts)
2. Rhythm
3. Heart rate,
4. PR interval/AV conduction
5. QRS interval
6. QT/QTc interval
7. Mean QRS electrical axis
8. P waves
9. QRS voltages
10. Precordial R-wave progression
11. Abnormal Q waves
12. ST segments
13. T waves
14. U waves
31. Standardization
The first step while reading ECG is to look for wheather
standardization is properly done.
Look for the vertical mark and see that the mark exactly covers
two big squares(10 mm or 1mV) on the graph.
Standard calibration
25 mm/s
0.1 mV/mm
33. RHYTHM
Evaluate the rhythm strip at the bottom of the 12-lead for
the following-
Is the rhythm regular or irregular?
Is there a P wave before every QRS complex?
Are there any abnormal beats?
34. The Heart Rate
1. Rule of 300/1500(Regular
rhythm)
2. 10 Second Rule
35. Rule of 300
Count the number of “big boxes” between two
QRS complexes, and divide this into 300.
(smaller boxes with 1500) for regular rhythms.
42. The PR Interval
Atrial depolarization
+
delay in AV junction
(AV node/Bundle of His)
(delay allows time for the
atria to contract before the
ventricles contract)
43. Normal PR interval
0.12 to 0.20 s (3 - 5 small squares).
Short PR – Wolff-Parkinson-White.
Long PR – 1st Degree AV block
45. Short PR Interval
WPW (Wolff-
Parkinson-White)
Syndrome
Accessory pathway
(Bundle of Kent)
allows early activation
of the ventricle (delta
wave and short PR
interval)
46. QRS INTERVAL(DURATION)
Normal QRS duration is 110-120 msec.
Intrinsic impairment of conduction in either the right or
the left bundle system (intra ventricular conduction
disturbances) leads to prolongation of the QRS interval.
With complete bundle branch blocks, the QRS interval
exceeds 120 ms in duration; with incomplete blocks, the
QRS interval is between 110 and 120 msec.
48. Bundle Branch Blocks
Conduction in the
Bundle Branches and
Purkinje fibers are seen
as the QRS complex on
the ECG.
Therefore, a conduction
block of the Bundle
Branches would be
reflected as a change in the
QRS complex.
Right
BBB
50. Right Bundle Branch Blocks
V1
For RBBB the wide QRS complex assumes a
unique, virtually diagnostic shape in those leads
overlying the right ventricle (V1 and V2).
“M shape”
52. Left Bundle Branch Blocks
For LBBB the wide QRS complex assumes a
characteristic change in shape in those leads
opposite the left ventricle (right ventricular leads -
V1 and V2).
Broad,
deep S
waves
Normal
55. QT INTERVAL
It includes the total duration of ventricular activation and
recovery.
When the interval is to be measured from a single lead, the lead
in which the interval is the longest, most commonly lead Avl,
V2 or V3, and in which a prominent U wave is absent should be
used.
The normal range for the QT interval is rate-dependent
A commonly used formula was developed by Bazett in 1920.
The result is a corrected QT interval, or QTc, defined by the
following equation:
QTc=QT/ RR
56. QT INTERVAL
The upper normal limit be set at 450 or even 460 msec.
The Bazett formula remains significantly affected by
heart rate and that as many as 30% of normal ECGs
would be diagnosed as having a prolonged QT interval
when this formula is used.
One formula that has been shown to be relatively
insensitive to heart rate is-
QTc= QT +1.75(HR-60)
60. The QRS Axis
The QRS axis represents overall direction of the
heart’s electrical activity.
Abnormalities hint at:
Ventricular enlargement
Conduction blocks (i.e. hemiblocks)
61. The QRS Axis
Normal QRS axis from -30° to
+90°.
-30° to -90° is referred to as a
left axis deviation (LAD)
+90° to +180° is referred to as a
right axis deviation (RAD)
65. The Quadrant Approach
1. QRS complex in leads I and aVF
2. Determine if they are predominantly positive or negative.
3. The combination should place the axis into one of the 4
quadrants below.
68. The Equiphasic Approach
1. Most equiphasic QRS complex.
2. Identified Lead lies 90° away from the lead
3. QRS in this second lead is positive or Negative
72. The “PQRST”
P wave - Atrial
depolarization
T wave - Ventricular
repolarization
QRS - Ventricular
depolarization
73. P wave
Always positive in lead I and II
Always negative in lead aVR
< 3 small squares ie 0.12sec in
duration
< 2.5 small squares(2.5mm) in
amplitude
Commonly biphasic in lead V1
Best seen in leads II
77. Notched/bifid (‘M’ shaped) P wave (P ‘mitrale’) in
limb leads
Left Atrial Enlargement
78. Left atrial enlargement
To diagnose LAE you can use the following criteria:
II > 0.04 s between notched peaks, or
V1 Neg. deflection > 0.04 s wide x 1 mm deep
Normal LAE
79. Left atrial enlargement
The P waves in lead II are notched and in lead V1 they have
a deep and wide negative component.
Notched
Negative deflection
83. QRS Complexes
Normal QRS patterns in the precordial leads follow an orderly
progression from right (V1) to left (V6).
In leads V1 and V2, left ventricular free wall activation
generates S waves following the initial r waves generated by
septal activation (an rS pattern).
As the exploring electrode moves laterally to the left, the R
wave becomes more dominant and the S wave becomes smaller
(or is totally lost).
In the leftmost leads (i.e., leads V5 and V6), the pattern also
includes the septal q wave to produce a qRs or qR pattern.
86. QRS Complexes
Nonpathological Q waves may present in I, III, aVL,
V5, and V6
Pathological Q wave > 2mm deep and > 1mm wide or
> 25% amplitude of the subsequent R wave
88. Left Ventricular Hypertrophy
Sokolow & Lyon Criteria
S in V1+ R in V5 or V6 > 35 mm
An R wave of 11mm (1.1mV) or more in lead aVL
is another sign of LVH
90. Right ventricular hypertrophy
To diagnose RVH you can use the following criteria:
Right axis deviation, and
V1 R wave > 7mm tall
91. ST Segment
ST Segment is flat (isoelectric)
Elevation or depression of ST segment by 1 mm or
more is significant.
“J” (Junction) point is the point between QRS and
ST segment
93. Variable Shapes Of ST Segment Elevations in AMI
Goldberger AL. Goldberger: Clinical Electrocardiography: A Simplified Approach. 7th
ed: Mosby Elsevier; 2006.
94. T wave
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.
96. U wave
U wave related to afterdepolarizations which
follow repolarization
U waves are small, round, symmetrical and
positive in lead II, with amplitude < 2 mm
U wave direction is the same as T wave
More prominent at slow heart rates
101. Acute Coronary Syndrome
Definition: a constellation of symptoms related to obstruction
of coronary arteries with chest pain being the most common
symptom in addition to nausea, vomiting, diaphoresis etc.
Chest pain concerned for ACS is often radiating to the left arm
or angle of the jaw, pressure-like in character, and associated
with nausea and sweating. Chest pain is often categorized into
typical and atypical angina.
102. Acute coronary syndrome
Based on ECG and cardiac enzymes, ACS is classified
into:
STEMI: ST elevation, elevated cardiac enzymes
NSTEMI: ST depression, T-wave inversion, elevated
cardiac enzymes
Unstable Angina: Non specific EKG changes, normal
cardiac enzymes
103. ECG
First point of entry into ACS algorithm
Abnormal or normal
Neither 100% sensitive or 100% specific for AMI
Single ECG for AMI – sensitivity of 60%, specificity 90%
Represents single point in time –needs to be read in context
Normal ECG does not exclude ACS – 1-6% proven to have AMI, 4%
unstable angina
104. GUIDELINES
Initial 12 lead ECG – goal door to ECG time 10min, read by experienced
doctor (Class 1 B)
If ECG not diagnostic/high suspicion of ACS – serial ECGs initially 15 -30
min intervals (Class 1 B)
ECG adjuncts – leads V7 –V9, RV 4 (Class 2a B)
Continuous 12 lead ECG monitoring reasonable alternative to serial ECGs
(Class 2a B)
105. Evaluating for ST Segment Elevation
Locate the J-point
Identify/estimate where the isoelectric line is noted to be
Compare the level of the ST segment to the isoelectric line
Elevation (or depression) is significant if more than 1 mm
(one small box) is seen in 2 or more leads facing the same
anatomical area of the heart
106. J point – where the QRS complex and ST segment
meet
ST segment elevation - evaluated 0.04 seconds (one
small box) after J point
The J Point
108. Evolution of AMI
A - pre-infarct (normal)
B - Tall T wave (first few minutes of
infarct)
C - Tall T wave and ST elevation
(injury)
D - Elevated ST (injury), inverted T
wave (ischemia), Q wave (tissue
death)
E - Inverted T wave (ischemia), Q wave
(tissue death)
F - Q wave (permanent marking)
114. NSTEMI:
ST depressions (0.5 mm at least) or T wave inversions ( 1.0
mm at least) without Q waves in 2 contiguous leads with
prominent R wave or R/S ratio >1.
Isolated T wave inversions:
can correlate with increased risk for MI
may represent Wellen’s syndrome:
critical LAD stenosis
>2mm inversions in anterior precordial leads
Unstable Angina:
May present with nonspecific or transient ST segment
depressions or elevations
119. Metabolic Factors and Drug Effects
Hyperkalemia produces a sequence of changes , usually
beginning with -
Narrowing and peaking (tenting) of the T waves.
AV conduction disturbances
Diminution in P-wave amplitude
Widening of the QRS interval
Cardiac arrest with a slow sinusoidal type of mechanism
("sine-wave" pattern)
Asystole.
123. Metabolic Factors and Drug Effects
Hypokalemia prolongs ventricular repolarization, often with
prominent U waves.
Hypocalcemia typically prolongs the QT interval (ST portion).
Hypercalcemia shortens it.
Digitalis glycosides also shorten the QT interval, often with a
characteristic "scooping" of the ST–T-wave complex (digitalis
effect).
131. SA Block
Sinus impulses is blocked within the SA junction
Between SA node and surrounding myocardium
Occures irregularly and unpredictably
Present :Young athletes, Digitalis, Hypokalemia,
Sick Sinus Syndrome
133. First Degree AV Block
Delay in the conduction through the conducting system
Prolong P-R interval
All P waves are followed by QRS
Associated with : Acute Rheumatic Carditis, Digitalis, Beta
Blocker, excessive vagal tone, ischemia, intrinsic disease in
the AV junction or bundle branch system.
134. Second Degree AV Block
Intermittent failure of AV conduction
Impulse blocked by AV node
Types:
Mobitz type 1 (Wenckebach Phenomenon)
Mobitz type 2
135. Mobitz type 1 (Wenckebach Phenomenon)
Mobitz type II
136. Third Degree Heart Block
CHB evidenced by the AV dissociation
A junctional escape rhythm at 45 bpm.
The PP intervals vary because of ventriculophasic sinus arrhythmia;
138. 30 bpm
• Rate?
• Regularity? regular
normal
0.10 s
• P waves?
• PR interval? 0.12 s
• QRS duration?
Interpretation? Sinus Bradycardia
139. 130 bpm
• Rate?
• Regularity? regular
normal
0.08 s
• P waves?
• PR interval? 0.16 s
• QRS duration?
Interpretation? Sinus Tachycardia
140. Premature Atrial Contractions
Deviation from NSR
These ectopic beats originate in the atria (but not in the
SA node), therefore the contour of the P wave, the PR
interval, and the timing are different than a normally
generated pulse from the SA node.
143. Atrial Fibrillation
Deviation from NSR
No organized atrial depolarization, so no normal P waves
(impulses are not originating from the sinus node).
Atrial activity is chaotic (resulting in an irregularly
irregular rate).
Common, affects 2-4%, up to 5-10% if > 80 years old
144. PSVT
Deviation from NSR
The heart rate suddenly speeds up, often triggered by a
PAC (not seen here) and the P waves are lost.
150. ECG in Valvular Heart Disease
Aortic Stenosis
LV hypertrophy which is found in approximately 85% of patients with severe AS.
T wave inversion and ST-segment depression in leads with upright QRS complexes
are common
Left atrial enlargement in more than 80% of patients
AF occurs in only 10% to 15% of AS patients.
Atrioventricular and intraventricular block in 5% of patients
152. Mitral Stenosis
Left atrial is found in 90% of patients with significant MS
and sinus rhythm.
AF is common with long-standing MS.
RV hypertrophy correlates with RV systolic pressure.
153. Mitral Regurgitation
Left atrial enlargement and AF
Electrocardiographic evidence of LV enlargement occurs
in about one third of patients with severe MR.
154. ECG Signs of Acute Pulmonary
Embolism
Sinus tachycardia:8-73%
P Pulmonale : 6-33%
Rightward axis shift : 3-66%
Inverted T-waves in right chest leads: 50%
S1Q3T3 pattern: 11-50% (S1-60%, Q3-53% ,T3-20%)
Clockwise rotation:10-56%
RBBB (complete/incomplete): 6-67%
AF or A flutter: 0-35%
No ECG changes: 20-24%
Am J Med 122:257,2009
155. Electrocardiogram from a 33-year-old man who presented with a left main
pulmonary artery embolism on chest CT scan. He was hemodynamically stable
and had normal right ventricular function on echocardiography. His troponin and
brain natriuretic peptide levels were normal. He was managed with
anticoagulation alone. On the initial electrocardiogram, he has a heart rate of
90/min, S1Q3T3, and incomplete right bundle branch block, with inverted or
flattened T waves in leads V1 through V4.
156. ACUTE PERICARDITIS
The electrocardiogram (ECG) is the most important
laboratory test for diagnosis of acute pericarditis
The classic finding is diffuse ST-segment elevation in all
leads except aVR and often V1.
The ST segment is usually coved upward
PR-segment depression is also common. PR depression
can occur without ST elevation and be the initial or sole
electrocardiographic manifestation of acute pericarditis.
The ECG reverts to normal during days or weeks.
160. CVA
Electrocardiographic
abnormalities are
observed in approximately
70% of patients with
subarachnoid hemorrhage.
ST-segment elevation
and depression, T wave
inversion, and pathologic
Q waves are observed
Peaked inverted T
waves and a prolonged
QT interval
161. Normal Variants
Numerous variations occur in subjects without heart disease.
T waves can be inverted in the right precordial leads in normal
persons-occurs in 1% to 3% of adults and is more common in
women(persistent juvenile pattern).
The ST segment can be significantly elevated in normal
persons, especially in the right and midprecordial leads.
The elevation begins from an elevated J point and is commonly
associated with notching of the downstroke of the QRS
complex.
This occurs in 2% to 5% of the population and is most
prevalent in young adults
163. Technical Errors and Artifacts
Artifacts that may interfere with interpretation can come
from movement of the patient or electrodes, electrical
disturbances related to current leakage and grounding
failure, and external sources such as electrical stimulators
or cauteries.
Misplacement of one or more electrodes is a common
cause for errors.
Significant misplacement of precordial electrodes.
164. ECG RULES
If we follow Professor Chamberlains 10 rules they'll
give you an understanding of what is normal:-
165. RULE 1
PR interval should be 120 to 200
milliseconds or 3 to 5 little squares
166. RULE 2
The width of the QRS complex should not
exceed 110 ms, less than 3 little squares
167. RULE 3
The QRS complex should be dominantly upright in
leads I and aVF
168. RULE 4
QRS and T waves tend to have the same general
direction in the limb leads
