1. BASICS OF ECG AND ITS
Dr. Mohd Shahabuddin Adil
DM ( Ist year Resident)
ELECTROCARDIOGRAM – Definition and importance
NORMAL ECG WITH WAVES AND INTERVALS
METHODS OF QT CORRECTION
STEPS FOR ECG INTERPRETATION
SOME ABNORMAL ECGS
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
ECG or EKG stands for electrocardiogram or
electrocardiograph 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
5. IMPORTANCE OF ECG
ECG can identify :
Arrhythmias (localising sites of origin and pathways)
Myocardial ischemia and infarction (severity and
Electrolyte disturbances (i.e. hyperkalemia,
Drug toxicity (i.e. digoxin and drugs which prolong
the QT interval)
6. FUNDAMENTAL PRINCIPLES
Transmembrane ionic currents are ultimately
responsible for the potentials that are recorded as an
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
7. Contraction of any muscle is associated with electrical
changes called depolarization, which are detected by
electrodes attached to the surface of the body.
Repolarisation is a phase of recovery/relaxation. It is
a slow process, and occurs simultaneously over
extensive portions of the muscle fiber.
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.
9. ECG LEADS
The standard ECG has 12 leads:
3 Standard Limb Leads (L I,LII, LIII)
3 Augmented Limb Leads (aVR, aVL, aVF)
6 Precordial Leads (V1, V2, V3, V4, V5, V6)
10. Standard limb leads
Each standard limb lead is 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
The positioning for leads I, II, and III were first given by
Lead I — This axis goes from shoulder to shoulder, with the
negative electrode placed on the right shoulder and the positive
electrode placed on the left shoulder (RA - LA). This results in a 0
degree angle of orientation.
11. Lead II — This axis goes from the right arm to the left leg, with
the negative electrode on the shoulder and the positive one on the
leg (RA – LL). This results in a +60 degree angle of orientation.
Lead III — This axis goes from the left shoulder with negative
electrode to the right or left leg with positive electrode (LA – LL).
This results in a +120 degree angle of orientation.
12. Augmented Limb Leads
There are three augmented unipolar limb leads.
These are termed unipolar leads because there is a single positive
electrode that is referenced against a combination of the other limb
electrodes. The positive electrodes for these augmented leads are
located on the left arm (aVL), the right arm (aVR), and the left leg
Limb leads, which are recorded from the elecrodes attached to the
limbs, can be thought of looking at the heart in a vertical plane i.e
from the sides or from the feet.
The aVL lead is at -30° relative to the lead I axis
aVR is at -150° and
aVF is at +90°.
14. Einthoven Triangle
Einthoven's triangle is an imaginary
formation of three limb leads in a triangle used
in electrocardiography, formed by the two
shoulders and the pubis. The shape forms an
inverted equilateral triangle with the heart at
16. Precordial leads
The Precordial Leads, or Chest Leads are labelled V1- V6
and are placed on the sternum travelling in a posterior
The six numbered precordial leads look at the heart in a
horizontal plane, from the front and left side.
V1 – 4th intercostal space on the RIGHT sternal border
V2 – 4th intercostal space on the LEFT sternal border.
V3 – BETWEEN V2 and V4
V4 – 5th intercostal space at left midclavicular line.
V5 – Same level of V4 at left anterior axillary line
V6 – Same level of V5 at left midaxillary line
18. Lead Groupings or Contiguous Leads are categories of
leads based on the area of the heart they examine:
Inferior - Leads II, III, aVF
“Look” down, towards the feet
Antero-septal - V1, V2
Overview the interventricular septum and anterior wall of
Anterior - V3, V4
Predominantly over anterior wall of left ventricle
Lateral - V5, V6, Leads I, aVL (High Lateral)
Examine lateral wall of left ventricle
Lead Groupings or Contiguous Leads
19. ECG paper
ECG paper is marked with a grid of small and large squares.
Each small square represents 40 milliseconds (ms) i.e 0.04 seconds
in time along the horizontal axis and each larger square contains
5 small squares, thus representing 200 ms i.e 0.20 seconds.
The ECG paper speed is ordinarily 25 mm/sec.
The amplitude, or voltage, of the recorded electrical signal is
expressed on an ECG in the vertical dimension and is measured
in millivolts (mV). On standard ECG paper 1mV is represented by a
deflection of 10 mm (1 small sqare = 0.1mv)
Calibration is said to be standard, if a signal of 1mV moves the
stylus vertically 1cm (2 large boxes).
21. NORMAL ECG – waves and intervals
The first structure to be depolarised during normal sinus rhythm is the
right atrium, closely followed by the left atrium. So the first electrical
signal on a normal ECG originates from the atria and is known as the P
P – wave is < 2.5 small squares(2.5mm) in amplitude and < 3
small squares i.e 0.12sec in duration.
Although there is usually only one P wave in most leads of an
ECG, the P wave is in fact the sum of the electrical signals from
the two atria, which are usually superimposed.
There is then a short, physiological delay as the atrioventricular
(AV) node slows the electrical depolarisation before it proceeds to
the ventricles. This delay is responsible for the PR interval, a
short period where no electrical activity is seen on the ECG,
represented by a straight horizontal or ‘isoelectric’ line.
22. Depolarisation of the ventricles results in usually the largest part
of the ECG signal (because of the greater muscle mass in the
ventricles) and this is known as the QRS complex.
The Q wave is the first initial downward or ‘negative’ deflection
The R wave is then the next upward deflection (provided it
crosses the isoelectric line and becomes ‘positive’)
The S wave is then the next deflection downwards, provided it
crosses the isoelectric line to become briefly negative before
returning to the isoelectric baseline.
23. In the case of the ventricles, there is also an electrical signal
reflecting repolarisation of the myocardium. This is shown as
the ST segment and the T wave. The ST segment is normally
isoelectric, and the T wave in most leads is an upright deflection of
variable amplitude and duration.
24. The PR Interval : The duration from start of P wave to
start of Q wave is PR interval. It is manifested by Atrial
depolarization + delay in AV junction (AV node/Bundle of His)
(delay allows time for the atria to contract before the
Normal range 120 – 200 ms or 0.12 to 0.20 sec (3 – 5 small
squares on ECG paper).
R – R interval : RR interval, the time elapsed between two
successive R-waves of the QRS signal on the
The RR interval is simply the time between successive
25. Heart rate – In an ECG, heart can be estimated by by rule of 300
for regular rhythms i.e Count the number of “big boxes” between
two QRS complexes, and divide this into 300.
Heart rate = 300 / No of big boxes between two QRS
10 second rule applies for estimation of heart rate for irregular
Count the number of beats present on the ECG during 10 seconds
i.e 50 big squares. Multiply them by 6 For irregular rhythms.
Heart rate =No of beats in an ECG during 10 seconds X 6
26. QT Interval :The duration from start of Q wave to end of T wave
is QT interval. It includes the total duration of ventricular activation
and recovery i.e it includes QRS complex, the ST segment, and the
The normal range for the QT interval is rate-dependent. The
faster the heart rate, the faster it must repolarize to prepare for
the next contraction; thus, the shorter the QT interval.
The QT interval is influenced by heart rate. The RR interval
preceding the QT interval should be measured for rate correction.
27. The normal value for the QTc in 440 t0 460msec.
QT prolongation is considered when the corrected QTc interval is
greater than 440 ms (men) and 460 ms (women), although
arrhythmias are most often associated with values of 500 ms or
Traditionally, lead II has been used for QT interval measurement
because in this lead, the vectors of repolarisation usually result in a
long single wave rather than discrete T and U waves
28. METHODS TO CORRECT THE QT INTERVAL
Several formulae may be used to correct the QT interval for the
biophysical effect of heart rate (QTc), but none is perfect.
The most commonly used formulae are :
1. Fridericia’s cube root formula (QTc) = QT/RR1/3
2. Bazett’s square root formula (QTc) = QT/RR1/2)
3. Framingham formula (QTc) = QT+0.154 (1−RR)
4. Hodges formula (QTc) = QT+0.00175 ([60/RR]−60)
5. Rautaharju formula (QTc) = QT−0.185 (RR−1)+k
(k=+0.006 seconds for men and +0 seconds for women)
Amongst the above formulaes Bazett’s formula is the more popular, but
Fridericia’s correction is preferred because it is more accurate at the
extremes of physiological heart rate.
30. Evolution of Torsades de pointes (TdP)
TdP, an uncommon polymorphic ventricular tachycardia, is
characterized by a gradual change in the amplitude and twisting of
the QRS complexes around the isoelectric line on an
TdP is associated with QTc prolongation, which is the heart-rate–
adjusted lengthening of the QT interval.
Blocking Ikr (delayed rectifier potassium current) leads to
prolongation of the ventricular action potential duration, leading
to an excess sodium influx or a decreased potassium
efflux.This leads to prolonged repolarization of the heart is
represented by a prolonged QT interval and can predispose a
patient to develop this life-threatening arrhythmia.
31. QT DISPERSION (QTd)
QT dispersion (QTd) is measured as the difference between the
longest and the shortest QT distances on the 12-lead surface ECG.
(maximum – minimum QT intervals).
Normal QTd values – 0.35s – 0.44s ( Ref : MD sulaiman et al.1997)
Corrected QT dispersion (QTcd) is calculated as the difference
between the maximum and the minimum corrected QT distances.
It is an indirect measure of spatial heterogeneity of repolarisation,
may be useful in assessing drug efficacy and safety.
Increased QTd indicates heterogeneity in ventricular repolarization,
which is associated with an increased risk of ventricular arrhythmia
32. Drugs known to cause QT prolongation and Torsades
de pointes : Class Examples
Antiarrhythmics Disopyramide, procainamide,
Macrolides Azithromycin, clarithromycin,
Fluoroquinolones Ciprofloxacin, levofloxacin,
Antifungals Fluconazole, ketoconazole,
Antipsychotics Haloperidol, thioridazine, ziprasidone
Antidepressants Citalopram, escitalopram,
Antiemetics Dolasetron, droperidol, granisetron,
Miscellaneous Cocaine, cilostazol, donepezil
34. ABNORMAL WAVES IN ECG
The U wave is a small (0.5 mm) deflection immediately following
the T wave
U wave is usually in the same direction as the T wave.
U wave is best seen in leads V2 and V3.
U -wave size is inversely proportional to heart rate: the U wave
grows bigger as the heart rate slows down
U waves generally become visible when the heart rate falls below
35. Prominent U waves most commonly found with: Bradycardia
and severe hypokalemia
Drugs associated with prominent U waves:
• Phenothiazines (thioridazine)
• Class Ia antiarrhythmics (quinidine, procainamide)
• Class III antiarrhythmics (sotalol, amiodarone)
36. STEPS FOR ECG INTERPRETATION
STEP 1 : Is the rhythm regular? Measuring the distance between
one R to the next can determine if that baseline measurement matches
all other R-to-R distances within a given amount of time, typically six to
STEP 2 : Calculate heart rate.
STEP 3 : Diagnose the P waves - Determine if the P waves are
present, upright and followed by the QRS segment.
If all three are within normal limits, chances are the electrical impulse
began in the SA node, as it should.
STEP 4 : Measure the P-R interval - A typical P-R interval is 0.12 to
0.20 seconds, with a prolonged P-R interval suggesting a blockage or
delay through the AV node.
37. STEP 5 : Measure the QRS segment - The normal duration of the
QRS segment is 0.04 to 0.10 seconds. A prolonged QRS segment
could signify a bundle branch block.
STEP 6 : Check the T wave. The T wave should be upright and
follow the QRS segment. Inverted T waves may indicate a lack of
oxygen to the heart, peaked T waves suggest hyperkalemia, flat T
waves may indicate low potassium, and a raised ST segment may
suggest a heart attack.
STEP 7 : Check the abnormal wave – If all the above normal
waves are present, look for abnormal wave like U wave.
38. STEP 8 : Determine the origin. With all the above information in
place, look for these elements.
Sinus: regular rhythm with 60-100 beats per minute; P waves
upright, round, and occurring before the QRS segment; normal P-R
interval; normal QRS duration.
Atria: Rhythm may or may not be regular; QRS segment is normal
with abnormal P waves (premature, flat, notched, peaked, inverted,
Ventricular: If the rhythm originates below the SA node, the QRS
segment will be wide and unusual with no P waves.
39. ECG rules
If we follow professor Chamberlains 10 rules they will give us
understanding of what is normal.
40. RULE 1 : PR interval should be 120 to 200 milliseconds or 3 to 5
little squares .
RULE 2 : QRS complex should not exceed 110 msec i.e less than 3
41. RULE 3 : QRS comples should be dominantly upright Lead I and
RULE 4 : QRS and T waves tend to have the same general
direction in the limb leads.
RULE 5 : All waves are negative in lead aVR.
RULE 6 :The R wave must grow from V1 to at least V4 and the S
wave must grow. from V1 to at least V3 and disappear in V6.
RULE 7 : ST segment should start isoelectric.
RULE 8 : The P waves should be upright in I, II, and V2 to V6
RULE 9 : There should be no Q wave or only a small q less than
0.04 seconds & less than 0.04 seconds.
RULE 10 : The T wave must be upright in I, II, V2 to V
44. BUNDLE BRANCH BLOCKS (BBB)
Conduction in bundle branches and purkinje fibers is seen are
seen as QRS complex on ECG.
Therefore, a conduction block of the bundle branches would be
reflected as a change in the QRS complex.
RIGHT BUNDLE BRANCH BLOCK
For RBBB the wide QRS complex
assumes a unique ,virtually
diagnostic shape in the leads
overlying right ventricle (V1 and
45. LEFT BUNDLE BRANCH BLOCK
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 ) – Broadened Deep S
46. 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
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
47. 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
48. J point – where the QRS complex and ST segment meet
ST segment elevation - evaluated 0.04 seconds (one small box) after J point
ST ELEVATION WITHOUT INFARCTION
• CONVEX – indicates acute injury
• CONCAVE – usually benign,if patient is asymptomatic
49. EVOLUTION OF MYOCARDIAL INFARCTION
• HYPERACTUTE AND TALL T –
WAVES First few minutes of
• TALL T WAVE AND ST ELEVATION –
• ELEVATED ST – Injury ; INVERTED
T – WAVE – Ischaemia ; Q WAVE –
• ST ELEVATION IMPROVES ; T
WAVE INVERSION – Ischaemia and
Q WAVE – Tissue death.
• Q WAVE PERSISTS AND T WAVE
NORMALISES – Permanent
50. MYOCARDIAL INFARCTION - FEW ECGs
Points to consider :
• ST elevation and Hyperacute T waves V2 – V4
• Q waves in V1 and V2
• These features indicate HYPERACUTE ANTEROSEPTAL STEMI
51. Points to consider :
• There are hyperacute T-waves in V2-6 (most marked in V2 and V3) with loss of R wave height.
• Normal sinus rhythm with 1st degree AV block
• These features indicate HYPERACUTE ANTERIOR STEMI
52. Points to consider :
• ST elevation in V2-6, Lead I and aVL.
• Reciprocal ST depression in III and AVF.
• These features indicate EXTENSIVE ANTEROLATERAL STEMI
53. Points to consider :
• ST elevation is present throughout the precordial and inferior leads (V1 To V6 and Lead II,III and aVF)
• There are hyperacute T waves, most prominent in V1-3
• These features indicate ANTEROINFERIOR STEMI
54. Points to consider :
• ST elevation is present in the Lead II,III and aVF)
• Reciprocal ST depression and T wave inversion in aVL
• These features indicate INFERIOR WALL STEMI
55. Points to consider :
• ST elevation is present in the high lateral leads (I and aVL)
• There is also subtle ST elevation with hyperacute T waves in V5-6.
• There is reciprocal ST depression in the inferior leads (III and aVF)
• These features points that there is infarction in the superior portion of the lateral wall of the left ventricle
(high lateral STEMI). indicate INFERIOR WALL STEMI
57. FIRST DEGREE AV BLOCK
Delay in the conduction through the conducting system
Uniformly Prolonged 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
58. SECOND DEGREE AV BLOCK
ECG patterns that describe the behavior of the PR intervals (in sinus rhythm) in
sequences with at least 2 consecutively conducted PR intervals in which a single P
wave fails to conduct to the ventricles.
Mobitz Type I (Wenckebach AV block)
Progressive prolongation of the PR interval culminating in a non-conducted P wave
PR interval is longest immediately before the dropped beat
PR interval is shortest immediately after the dropped beat
59. Mobitz Type II (Hay AV block)
Intermittent non-conducted P waves without progressive prolongation of the PR
PR interval in the conducted beats remains constant.
P waves ‘march through’ at a constant rate.
RR interval surrounding the dropped beat(s) is an exact multiple of the preceding RR
interval (e.g. double the preceding RR interval for a single dropped beat, treble for
two dropped beats, etc).
Arrows indicated ‘dropped’ QRS complexes (i.e. non-conducted P waves).
60. Points to consider :
Rhythm – irregularly irregular
Rate – Atrial rate very fast and chaotic
P wave – Not discernible
P-R interval – None
QRS complex – Normal
61. Points to consider :
Rate – Heart rate in atrial flutter is usually fast
P wave – classical saw tooth pattern, with atria firing at a rate of 200 – 350 /
P-R interval – None
QRS complex – usually narrow
P wave to QRS ratio – 2:1 ; 3:1 ; 4:1