HOW TO READ ECG

Part 1- Basics of ECG

Willem Einthoven (1901)
 Electrocardiography- The process

Electrocardiograph- the machine

Electrocardiogram- The graph/

Tracing
Electrocardiograph- the machine
ElectrocardioGRAM

Electrocardiograph- the machine

ElectrocardioGRAM

Electrocardiograph- the machine

 ECG paper measurements
 Standard speed of ECG paper = 25 mm/sec.
 ECG paper measurements
• Thin Lines: 1 mm intervals or (1/25)sec=0.04 sec
• Thick lines: 5 mm intervals or (5×0.04)sec = 0.2sec
• 1 thick lined box (5 small boxes) = 0.2 sec or
5mm
• 5 thick lines boxes (25 small boxes)= (0.2×5)sec =
1 sec
• STANDARD HEIGHT: - 10 mm = 1 mV, Hence 1
mm (1 small square)= 0.1 mV
CARDIAC CONDUCTION PATHWAY
SA Node
Internodal
(Pacemaker
pathways
of heart)

Bundle of
AV Node
His

Right and
Purkinje
Left Bundle
Fibres
Branches

Myocardium
CARDIAC CONDUCTION PATHWAY
 BASICS OF ECG WAVES
1. SA Node • Too small to be detected
Depolarisation • NO DEFLECTION on ECG (= Not seen in ECG)

• Atrial Depolarisation
2. P wave • Right atrial followed by left atrial
depolarisation

3. PR segment • AV Node + Bundle of His depolarisation

• Ventricular Depolarisation (Right and

4. QRS complex Left vent. simultaneously)
• Atrial Repolarisation
5. ST Segment & T
• Ventricular Repolarisation
wave
6. U wave (Not
• Late repolarisation of papillary muscle
seen regularly)
CARDIAC CONDUCTION PATHWAY
 Calculation of Heart rate
 Heart rate = Ventricular rate per min.
 1 sec = 25 mm = 25 small squares
 Hence, 1 min = 60 sec = (25×60) = 1500 small
squares = (1500÷5) = 300 Big Squares.
 Heart rate = Ventricular rate = (1500 ÷ R-R
interval in terms of small Square) = (300 ÷ R-R
interval in terms of Big Square)
 Prerequisite: - Rhythm should be regular, i.e.
R-R intervals should be equal.
Tachycardia Bradicardia

HR >100 HR < 60

RR < 3 RR > 5
Large sqr Large sqr
 RR interval = 14 small sqr
Hence, HR = (15oo÷14) = 107.14
RR < 3 Large sqr = Tachycardia
 ECG LEADS
 It’s called as “12 lead
ECG”
 6 LIMB LEADS: - To
detect vertical
electrical activity of
the heart.
 6 CHEST (or
PRECORDIAL)
LEADS: - To detect
horizontal
electrical activity of
the heart.
 6 Limb Leads
 3 Bipolar Leads  3 Unipolar leads
L-1, L-2, L-3 aVL, aVF, aVR
6 Limb Leads
 6 Precordial Leads (V1 to V6)
•V1 4th intercostal space immediately to the right
of the sternum.
•V2 4th intercostal space immediately to the left
of the sternum.
•V3 Midpoint between V2 and V4.
•V4 5th intercostal space on left midclavicular
line.
•V5 same horizontal level as V4, on left anterior
axillary line.
•V6 same level as V5, on left mid axillary line.
Wall specific ECG Leads
Additional Lead placement
(Beyond 12 leads)
 DESCRIPTION OF DIFFERENT ECG
WAVES, SEGMENTS and INTERVALS
 P Wave
Characteristics of the Normal Sinus P
Wave
 Morphology
• Smooth contour
• Monophasic in lead II
• Biphasic in V1
• P waves should be upright in leads I and II,
inverted in aVR
 Duration
• < 0.12 s (<120ms or 3 small squares)
Amplitude
• < 2.5 mm (0.25mV) in the limb leads
• < 1.5 mm (0.15mV) in the precordial leads
NORMAL P WAVE
 Abnormalities of P wave
 P Mitrale
The presence of broad, notched (bifid) P
waves in lead II is a sign of left atrial enlargement,
classically due to mitral stenosis. P wave width
>2.5 small sqr.
 P Pulmonale
The presence of tall, peaked P waves in lead
II is a sign of right atrial enlargement, usually due
to pulmonary hypertension (e.g. cor
pulmonale from chronic respiratory disease). P
wave height >2.5 small sqr
 Multifocal atrial tachycardia (MAT)
If ≥ 3 different P wave morphologies are
seen and the rate is ≥ 100, then MAT is diagnosed
 Abnormalities of P wave
 Absent P wave
1. Junctional Rhythm
2. Atrial Fibrillation (AF)
3. Paroxysmal Supraventricular
tachycardia (PSVT)
 SEGMENT vs INTERVAL in ECG
Segment Interval

 A flat line (Isoelectric)  A time duration that

between two waves on an includes one segment and
ECG that are at baseline one or more waves. For
amplitude. For example, the example, the PR interval is
PR segment is the flat line the time between the start of
between the end of the P atrial activation
wave and the start of the QRS (depolarization) and the start
complex. of ventricular activation
(depolarization).
 PR Segment and PR Interval
 PR segment represents AV Nodal delay
 Although PR interval comprises of P wave (i.e., atrial
depolarisation) and PR segment, the main contributor
is AV Nodal delay.
 AV node is the slowest conducting tissue.
 Normal duration of PR Interval: - 0.12-0.2 sec =
3-5 small square
 Prolonged PR Interval (> 5 Small
Square)
 AV Block
1. AV nodal edema/ inflammation: - ex- Acute
rheumatic fever (PR prolongation is minor Jones
criteria)
2. Drug Induced: - β Blocker, Non DHP CCB
(Verapamil, Diltiazem), Digoxin
3. Dyselectrolytemia: - Both Hyper & Hypo kalemia
4. AV Nodal infiltration with poor conductor of
current: - Amyloidosis
 Shortened PR Interval (< 3 small
square )
 When atrial impulse (Impulse generated from SA
node) bypass AV node via accessory pathways.
 Accessory pathways: - These pathways conduct
electrical impulse faster than AV node.
 Accessory pathways: -
 James pathway/ James Tract
 Bundle of Kent/ Tract of kent
 Bundle of Kent [WPW syndrome
(Wolf Parkinson White)]
 2 Types: - Type A and
Type B
 Most common is Type
A, where it connects
Left Atrium to Left
Ventricle.
 Results in pre-
excitation of Left
ventricle Slurred
upstroke of QRS
complex, known as
“Delta wave”
James Tract [LGL Syndrome (Lown Ganong
Levine)]
 James tract
directly
connected to
Bundle of His,
bypassing the AV
Node.
 LGL syndrome
ECG: - Shortened
PR Interval with
Normal QRS
Complex
Shortened PR interval (< 3 small sqr) and Normal QRS (No
Delta wave) = LGL syndrome
Shortened PR interval (< 3 small sqr) and Delta wave = WPW
syndrome
Shortened PR interval (< 3 small sqr) and Delta wave = WPW
syndrome
 QRS Complex: - Ventricular
Depolarisation
 QRS complex is the largest deflection in the ECG
 Represents activation (Depolarisation) of the
ventricles.
 QRS complex is recorded only when the impulse has
spread from the Purkinje fibers to the myocardium.
 Depolarization of the whole myocardium can vary
from 0.08 to 0.10 seconds or longer. This duration
corresponds to the width of the QRS complex in the
ECG.
 Hence normal width of QRS complex= 0.08-0.10 sec =
Almost 2-3 small sqr
 QRS Complex: - Ventricular
Depolarisation
 What to look for?
 Width [Narrow (= Normal) or Wide (> 3 small
sqr)]
 Morphology
 Cardiac Axis
Wide QRS (>3 small sqr): - If
both ventricles are not depolarising
simultaneously
 Idioventricular rhythm
 Ventricular depolarisation is controlled by a pacemaker
which is distal to Bundle of His
 LBBB/ RBBB (Left or Right Bundle Branch
Block)
 Dyselectrolytemia (Hyperkalemia)
 Ventricular pre-excitation: - WPW syndrome
 Pacemaker generated beat
 Drug toxicity: - Cocaine
 Abnormal QRS Morphology

Ventricular hypertrophy
 RVH (Pulmonary stenosis, Pulmonary arterial HTN)
 LVH (AS, Systemic HTN)

 Bundle Branch Block

 RBBB

 LBBB
 RVH
 Diagnostic criteria
 Right axis deviation of +110° or more.
 Dominant R wave in V1 (R > 7mm tall or R/S ratio
> 1).
 Dominant S wave in V5 or V6 (S > 7mm deep or
R/S ratio < 1).
 QRS duration < 120ms (i.e. changes not due to
RBBB).
 LVH
 There are numerous voltage criteria for diagnosing LVH.
 The most commonly used are the Sokolov-Lyon criteria:
S wave depth in V1 or V2 + tallest R wave height in
V5-V6 > 35 mm (> 7 Large sqr).

 Other criteria: -
 R wave in V4, V5 or V6 > 26 mm (almost 5 large sqr)
 R wave in aVL > 11 mm (almost 2 large sqr)
 RBBB
 QRS duration > 120ms
 RSR´ pattern or M
pattern or Rabbit ear
pattern in V1-3
 Wide, slurred S wave in
lateral leads (I, aVL, V5,
V6)
 LBBB
 QRS duration ≥ 120ms
 Dominant S wave in V1
 Broad monophasic R wave in leads I, aVL, V5-6
 Absence of Q waves in lateral leads
 Prolonged R wave peak time > 60ms in leads V5-6
 W pattern in V1 and M pattern in V6
 Cardiac Axis
 Normal cardiac axis
= (-30°) to (+ 110°)
• Left Axis
Deviation = QRS
axis less than -30°.
• Right Axis
Deviation = QRS
axis greater than
+110°.
• Extreme Axis
Deviation = QRS
axis between -90°
and 180° (AKA
“Northwest Axis”).
 Measurement of cardiac axis
 The most efficient way to estimate axis is to look
at LEAD I and LEAD aVF. (The Quadrant Method)
 Examine the QRS complex in each lead and
determine if it is Positive, Isoelectric (Equiphasic) or
Negative.
Measurement of cardiac axis
 Causes of axis deviation
RAD LAD
 Right ventricular hypertrophy  Left anterior fascicular
(Most common cause) block (Most common
 Acute lung disease (e.g. cause)
Pulmonary Embolus)  Left bundle branch block
 Chronic lung disease (e.g. COPD)  Left ventricular
 Dextrocardia hypertrophy
 Normal in children or thin adults  Inferior MI
with a horizontally positioned  Paced rhythm
heart  Wolff-Parkinson White
 Left posterior fascicular block syndrome
 Lateral myocardial infarction
 WPW syndrome
 Causes of axis deviation
 Extreme Axis Deviation
 Wrong lead placement (Most common)
 Dextrocardia
 Emphysema
 Ventricular pacing
 Ventricular arrhythmia
 Hyperkalemia
ST Segment & T wave: - Ventricular
Repolarisation
 ST Segment
 Normally it is the flat, isoelectric section of the ECG
between the end of the S wave (the J point) and the
beginning of the T wave.
 It represents the interval between ventricular
depolarization and repolarization.
ST Segment abnormalities
 Abnormal ST Segment is Non-isoelectric = Not flat.
 There can be ❶ST elevation or ❷ST depression.
 The most important cause of ST segment abnormality
(elevation or depression) is myocardial ischemia or
infarction.
 ST Elevation
 Acute myocardial infarction
 Coronary vasospasm (Printzmetal’s angina)
 Pericarditis
 Benign early repolarization (BER)
 Left bundle branch block
 Left ventricular hypertrophy
 Ventricular aneurysm
 Brugada syndrome
 Ventricular paced rhythm
 Raised intracranial pressure
 Takotsubo Cardiomyopathy
Significant ST Elevation
Non-Ischemic ST Elevation
 ST elevation in V2-6, L-I, and aVL.
 Reciprocal ST depression in III and AVF.

Anterolateral STEMI
 ST Depression
Causes of ST depression: -
Myocardial ischemia / NSTEMI (Non ST
Elevation MI)
Reciprocal change in STEMI
Digoxin effect
Hypokalaemia
 ST Depression
 Horizontal or downsloping ST depression ≥ 0.5 mm
at the J-point in ≥ 2 contiguous leads indicates
myocardial ischemia
 Reciprocal change has a morphology that resembles
“upside down” ST elevation and is seen in leads
electrically opposite to the site of infarction
Reciprocal leads
 ST depression in almost all leads
 ST depression due to subendocardial ischemia is usually widespread

NSTEMI
 T Wave: - Ventricular
Repolarisation
 Usually same direction as QRS.
 It has asymmetrical limbs (Contrary to P wave, which
has symmetrical limbs)
 Normal T wave morphology:
i. Upright in I, II, V3-V6, inverted in aVR
ii. May be upright, flat or biphasic in III, aVL,
aVF, V1, V2
iii. T wave inversion may be present in V1-V3 in
healthy young adults (juvenile T waves)
 Amplitude < 5mm in limb leads, < 10mm in precordial
leads (10mm males, 8mm females)
Normal T wave
 T wave abnormalities
 Peaked T waves: - Hyperkalemia
 Hyperacute T waves: - Broad, asymmetrically peaked,
seen in the early stages of ST-elevation MI (STEMI),
and often precede the appearance of ST elevation and
Q waves
 Inverted T waves: - Pathological T wave inversion is
usually symmetrical and deep (>3mm)
Peaked T vs Hyperacute T
 Inverted T waves
 Normal finding in children
 Persistent juvenile T wave pattern
 Myocardial ischemia and infarction (including
Wellens Syndrome)
 Bundle branch block
 Ventricular hypertrophy (‘strain’ patterns)
 Hypertrophic cardiomyopathy
 Pulmonary embolism
 Raised intracranial pressure
T wave inversion with Q waves due to recent MI (But
not an acute MI)
 QT Interval
 It is a measure of the time between the start of
the Q wave and the end of the T wave
 QTc:
QT interval is affected by heart rate. It becomes
longer when the heart rate is slower and shorter
when the heart rate is faster. The QT interval
therefore should always be corrected for heart
rate.
 Corrected QT (QTC) = Bazett's Formula = QT
Interval / √ (RR interval)
 Normal duration= (0.4 ± 0.04) sec
 Prolonged QTc
 Acquired conditions
 Drugs (quinidine, procainamide, disopyramide,
amiodarone, sotalol, dofetilide, azimilide, phenothiazines,
tricyclics,lithium)
 Hypomagnesemia
 Hypocalcemia
 Marked bradyarrhythmias
 Intracranial hemorrhage
 Myocarditis
 Mitral valve prolapse
 Myxedema
 Hypothermia
 Liquid protein diets
 Congenital disorders
 • Romano-Ward syndrome (normal hearing)
 • Jervell and Lange-Nielson syndrome (deafness)
 Shortened QTc
 Hypercalcemia
 Hyperkalemia
 Digitalis effect
 Acidosis
 Vagal stimulation
 Hyperthyroidism
 Hyperthermia
 Q Wave
 How to Identify: - A Q wave is any negative
deflection that precedes an R wave.
 Under normal circumstances, Q waves are not
seen in the right-sided leads (V1-3)
 Normal Q waves: Small Q waves (duration < 0.03
seconds)
 Commonly seen in most leads, except aVR, V1-V3
 Pathological Q wave
 > 40 ms (1 mm) wide
 > 2 mm (>2 small sqr) deep
 > 25% of depth of QRS complex
 Seen in leads V1-3
 Pathological Q waves usually indicate current or prior
myocardial infarction.
 If the QRS consists exclusively of a negative deflection, that
defection is considered a Q wave, but the complex is
referred to as a “QS” complex
 For Q-wave myocardial infarction, Q wave changes must be
present in at least 2 contiguous leads and must be > 1 mm
in depth.
Pathological Q waves in L-II, L-III, aVF with ST elevation
due to acute MI