ECG

An overview

Compiled by
Abubakkar Siddique
3rd professional part 2 MBBS
Burdwan medical college and hospital
A heartfelt thanks to Dr Avijit Sir for guiding us in doing this.
Special Thanks to
Anjan Sain, Arijit Sen, Aditi Mandal, Girin Ray, Golam Murshed, j lalvenhimi, Masud Alam, Nandita Das, Nilambar Manik,
Saheli Sarkar, Sohail ansary, Students of Group A and my fellow Batchmates.

Contents
1. Basics of ECG 4-16

2. Atrial fibrillation and flutter 17-20

3. AV Blocks 21-31

4. Short PR interval 32-35

5.Supra ventricular tachycardia 36-37

6. Bundle branch block 38-40

7.Ventricular premature complex 41-43

8. Abnormalities in P waves 44-47

9. Left Ventricular hypertrophy 48-50

10. Right ventricular hypertrophy 51-53

11. Acute Coronary Syndrome 54-65

12. Practice ECGs including ECGs Of Department of Medicine BMC&H 66-94

13. Commonly asked question in ECG Table 95-96

2
A 29 Year old Male presented With history of presyncope(Sudden blackouts
while standing up from sitting posture), Coincidentally during checking his
spO2 in pulse oximeter his friend found that he is having a pulse of 46/min,
He went to a young MBBS practitioner, the doctor ordered an ECG and
then prescribed beta agonist and told him to have Tea, being not satisfied
he went to a cardiologist and the Cardiologist again ordered an ECG with
long lead 2. The ECG is as follows, What is your diagnosis and what is the
Management?

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4
Leads

5
Generation of ECG complex in Lead 2

6
Rate: Regular? Or Irregular?
Rhythm: Regular? Sinus? Every P wave followed by QRS?
Drop beats?
Axis:
Check for individual waves:
P wave: Duration? Height?
PR interval: Shortened? Increased?
QRS Complex: 2.5-3 SS width? Normal voltage?
Q Wave in V5, V6? Normal depth and width?
Pathological Q wave in?
R wave progression in chest leads?
QT Interval?
ST segment?
T wave:
height?

7
How to calculate rate?
See if the QRS complex are regular or not.
If regular then count the number of small squares between the R waves, lets say its X
ventricular rate= 1500/X
If its irregular then count the QRS complex between 30 large square(30 large aquare=6 second), lets say its Y,
Heart rate= Y*10

Pearl- Irregularly irregular QRS complexes seen in 3 condition

1. atrial fibrillation
2. Multifocal atrial tachycardia( P waves will be of different morphology)
3. Atrial flutter with variable AV blocks

How to calculate axis of ventricular depolarization?

Calculate R-S in lead 1 and avF then plot the value in the hexaxial reference system graph(shown below) positive value in lead 1 is plotted in the right side similar
to XY axis plotting system, but positive value in lead avF is plotted in the downward position unlike in XY axis system. Then draw a line from the centre joining the
perpendicular drawn from two points and the line is your QRS axis.

PR interval is Suppose my R-S

interval between value in lead 1 is
start of P wave and
+2 and in avF is
beginning of q
wave, it should -3 then the plot
have been named will be like this.
PQ interval, it’s a
misnomer

8
 Right Axis Deviation:
Left Axis Deviation:
Right ventricular hypertrophy
Left ventricular hypertrophy
Acute right ventricular strain, e.g. due to pulmonary embolism
P wave- <3 ss(120 ms), height- <2.5 mm in limb leads, <1.5 mm in chest leads Left bundle branch block
Lateral STEMI
P pulmonale- >2.5 mm vertical height, p mitrale- >3 mm duration Inferior MI
Chronic lung disease, e.g. COPD
Ventricular pacing /ectopy
PR interval- 3-5 ss(.12-.20 s) Hyperkalaemia
Wolff-Parkinson-White Syndrome
q wave- <1 ss duration and depth. Sodium-channel blockade, e.g. TCA poisoning
Primum ASD – rSR’ pattern
QRS- 2-2.5 ss(80-100 ms) Wolff-Parkinson-White syndrome
Left anterior fascicular block – diagnosis
QT interval- .36-.44 s(9-11 ss), inverse relation to electrolytes. Dextrocardia
of exclusion
Ventricular ectopy
ST segment-( end of S and start of T)- isoelectric segment. Horizontally orientated heart – short,
Secundum ASD – rSR’ pattern
T wave- height of T wave <5 mm in limb leads and <10 mm in chest leads. squat patient
Normal paediatric ECG
Normal axis -30 to +110 degree Left posterior fascicular block – diagnosis of exclusion
Left Axis Deviation = QRS axis less than -30°. Vertically orientated heart – tall, thin patient
Right Axis Deviation = QRS axis greater than +90°.
Extreme Axis Deviation = QRS axis between -90° and 180° (AKA “Northwest
Extreme Axis Deviation:
Axis”).
Ventricular rhythms – e.g. VT, Accelerated idioventricular rhythm, ventricular
ectopy
Hyperkalaemia 9
Severe right ventricular hypertrophy
10
Calculate the rate, Rhythm, Axis, PR interval, Duration
of QRS complex.

11
LAD

12
RAD

13
P Wave-
✓ Signifies atrial depolarization;
✓ Best visualized in- lead II , V1;
✓ If present- sinus rhythm;
✓ Height – 2.5mm or 0.25mV
✓ Width – 2.5mm or 0.1s.
✓ P-Pulmonale- Tall and peaked P Waves(>2.5mm):-Seen in- I. Severe pulmonary disease and consequent Right atrial hypertrophy.
✓ P-Mitrale- Wide and notched P wave, notching is significant if distance b/w two peaks of P wave crosses 1mm. It indicates mitral valve disease and
consequent left atrial hypertrophy.
✓ ABSENT P WAVE- IN- AF, SA block, nodal rhythm.
✓ INVERTED P WAVE-Seen in- Wrong electrode placement, dextrocardia and retrograde atrial activation (as seen in nodal rhythm).
✓ DIPHASIC OR BIPHASIC P Wave- Normally seen in V lead with terminal shallow negative component; if the negative component is prominent it indicates
left atrial hypertrophy.
QRS COMPLEX
✓ Q wave signifies- depolarization of ventricular septum from left to right side.
✓ R wave – Depolarization of ventricles. Initially anteroseptal portion is depolarized followed by major muscle mass.
✓ S wave- Depolarization of posterobasal part of left ventricle, pulmonary conus and superior-most part of ventricular septum.
✓ Height of QRS complex is different in different lead and also depends upon the position of heart and degree of abnormality.
✓ Duration- <3 mm(Wider in – BBB,VT,Hyperkalemia),
✓ LOW VOLTAGE QRS COMPLEX- In limb leads <5mm and in chest leads <10mm. common causes are-
• Incorrect standardization
• Obesity or thick chest wall
• Emphysema
• Myxoedema
• Pericardial effusion
✓ HIGH VOLTAGE QRS COMPLEX- Tall QRS complex and signifies RVH and LVH( Depending upon leads).
✓ Q WAVE-
• Width- 1mm
• Height- 2mm
• Pathological Q- length>2mm, width>1mm.
• Found in old MI.
✓ R WAVE-
• Duration- <2.5mm
• Length- In aVL <13mm , aVF <20mm , V5-6 <25mm , in V1<7mm
✓ RSr OR rSR PATTERN-
• Seen in bundle branch block. 14
• Depending upon in which lead this pattern is present it is determined that it is LBBB OR RBBB.
PR INTERVAL
✓ From beginning of P Wave to beginning of QRS complex.
✓ Normal duration- 0.12-0.20 second or 3mm-5mm.
✓ INCRESED PR INTERVAL- In first degree heart block, rheumatic fever, IHD.
✓ DECREASED PR INTERVAL- Wolff-Parkinson-White syndrome, AV nodal rhythm.
QRS INTERVAL
✓ From beginning of Q wave to termination of S wave.
✓ Normal duration- 0.10sec or 2.5mm
✓ QRS interval >0.12 sec =Complete bundle branch block
✓ 0.12sec>QRS interval>0.10 sec= Incomplete bundle branch block.
T WAVE
✓ Produced d/t ventricular repolarization,
✓ Normally upright except in leads III, aVR ,V1-2
✓ Tall peaked T wave- hyperkalaemia, acute subendocardial ischemia or infarction
✓ Low or inverted T wave- CHD or myocardial ischemia.
✓ Flat T wave- In thick chest wall, emphysema, myocardial ischemia, myxoedema, hypokalemia.
U WAVE
✓ After T and before P.
✓ D/t slow repolarization of Purkinje fibres, papillary muscles and iv septum.
✓ Usually best seen in- V2-4 .
✓ Prominent U- In hypokalemia
✓ Inverted U- CHD, HHD, Acute pulmonary thromboembolism, IC Haemorrhage.
Q-T INTERVAL
✓ From beginning of Q wave to end of T wave.
✓ Total duration of ventricular systole
✓ Duration- 0.35sec- 0.44 sec/ 9 -11mm
✓ Prolonged Q-T INTERVAL- Hypocalcemia, hypokalemia, AMI, QUINIDINE THERAPY, CCF, hypothermia
✓ Shortened Q-T INTERVAL- Hypercalcemia, digitalis therapy, vagal stimulation, hyperthermia.

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ST SEGMENT-
✓ From end of QRS complex to beginning of T wave.
✓ Usually isoelectric but varies in pathological conditions,
✓ T-P Segment is taken as isoelectric line and diagnosis of any depression in ST segment is made with reference to T-P
segment.
✓ J POINT- The point where QRS complex end and ST segment begins.
✓ J Point is evaluated for ST segment deviation.
✓ ST segment represents time b/w ventricular depolarization and repolarization,
✓ ST ELEVATION-
• AMI
• Prinzmetal’s angina
• Ventricular aneurysm
• Pericarditis
✓ ST DEPRESSION-
• Angina pectoris
• Ventricular hypertrophy with strain
• Digitalis effect
• Acute subendocardial infarction
✓ SOME ONELINERS-
• Elevated ST with convexity upwards- AMI, LVA
• Elevated ST with concavity upwards- Acute pericarditis
• Sagging/ plane/ oblique depression- CAD(Angina)
• Depressed with upward convexity- Strain patterns in VHs.
• Depressed with mirror image of correction mark- Digitalis effect.

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 Atrial fibrillation and Atrial flutter
•Features of Atrial flutter
•Narrow complex tachycardia
•Regular atrial activity at ~250-350 bpm
•Loss of the isoelectric baseline
•“Saw-tooth” pattern of inverted flutter waves in leads II, III,
aVF
•Upright flutter waves in V1 that may resemble P waves
•Ventricular rate depends on AV conduction ratio (see below)

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18
Atrial fibrillation

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Symptoms and signs:
Management of A fib:
❑ Symptoms attributable to atrial fibrillation are highly variable.
When atrial fibrillation is due to an acute precipitating event
In some patients (about 30%) it is an incidental finding, whilst
such as alcohol toxicity, chest infection or hyperthyroidism,
others attend hospital as an emergency with rapid palpitations
the provoking cause should be treated. Strategies for the
dyspnea and/or chest pain following the onset of atrial
acute management of AF are:
fibrillation. When caused by rheumatic mitral stenosis, the
R: Rate control: IV Esmolol/IV verapamil
onset of atrial fibrillation results in considerable worsening of
A: Anticoagulant (Oral dabigatran, Rivaroxaban, If due to RHD and
cardiac failure.
subsequent MS A fib has developed then Warfarin is used)
❑ The patient has a very irregular pulse, as opposed to a
C: Rhythm Control by IV Ibutilide/ Amiodarone, Chemical
basically regular pulse with an occasional irregularity (e.g.
cardioversion.
extrasystoles) or recurring irregular patterns (e.g. Wenckebach
E: Electrical cardioversion by DC shock 200 j biphasic
block). The irregular nature of the pulse in atrial fibrillation
To prevent 1 degree A fib episodes oral amiodarone and ablation
is maintained during exercise.
catheter is used.
❑ The ECG shows fine oscillations of the baseline (so-called
If pt have CHF and A fib then digoxin is used and esmolol is
fibrillation or f waves) and no clear P waves. The QRS rhythm
contraindicated.
is rapid and irregular. Untreated, the ventricular rate is usually
120–180/minute, but it slows with treatment.
Management of Atrial flutter:
The clinical classification of atrial fibrillation includes first
IV esmolol(Rate control)/IV Verapamil
detected, paroxysmal (stops spontaneously within 7 days),
Anticoagulation to prevent 1 degree pulmonary embolism
persistent (requires cardioversion to stop), and permanent
Rhythm control by IV Ibutilide if it fails then Synchronized DC Shock 25-
(no spontaneous or induced cardioversion) forms of the
50 J biphasic electrical cardioversion.
arrhythmia and is helpful for the decision-making between
rhythm restoration and rate control. Atrial fibrillation may be
asymptomatic and the ‘first detected episode’ should not be
regarded as necessarily the true onset.

In short A fib and A flutter will lead to palpitation, loss of

consciousness SBP decreases and rapid pulse will be there

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 AV Blocks

Primary AV block
Diagnostic criteria:
PR interval > 200ms (five small squares)
There is delay, without interruption, in conduction from atria to ventricles
‘Marked’ first degree heart block is present if PR interval > 300ms
Causes of First Degree Heart Block:
Increased vagal tone
Athletic training
Inferior MI
Mitral valve surgery
Myocarditis (e.g. Lyme disease)
Electrolyte disturbances (e.g. Hyperkalaemia)
AV nodal blocking drugs (beta-blockers, calcium channel blockers, digoxin, amiodarone)
May be a normal variant
Clinical significance:
As an isolated finding this is a benign entity that does not cause haemodynamic instability
No specific treatment is required

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Sinus bradycardia with 1st degree AV block
PR interval > 300 ms

Marked first degree heart block

PR interval > 300 ms, P waves are buried in the preceding T wave

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 Second degree AV Block
Definition of Mobitz I block (Wenckebach phenomenon)

Progressive prolongation of the PR interval culminating in a non-conducted P wave:

PR interval is longest immediately before dropped beat
PR interval is shortest immediately after dropped beat

Other Features:
The P-P interval remains relatively constant
The greatest increase in PR interval duration is typically between the first and second beats of the
cycle
The RR interval progressively shortens with each beat of the cycle
The Wenckebach pattern tends to repeat in P:QRS groups with ratios of 3:2, 4:3 or 5:4
Mechanism:
Mobitz I is usually due to reversible conduction block at the level of the AV node
Malfunctioning AV nodal cells tend to progressively fatigue until they fail to conduct an impulse. This is different to cells of the His-Purkinje system which tend to fail suddenly and
unexpectedly (i.e. producing a Mobitz II block)
Causes of Wenckebach Phenomenon:
Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone
Increased vagal tone (e.g. athletes)
Inferior MI
Myocarditis
Following cardiac surgery (mitral valve repair, Tetralogy of Fallot repair)
Clinical Significance:
Mobitz I is usually a benign rhythm, causing minimal haemodynamic disturbance and with low risk of progression to third degree heart block
Asymptomatic patients do not require treatment
Symptomatic patients usually respond to atropine
Permanent pacing is rarely required

23
 Second degree AV Block

Mobitz I AV block
Progressive prolongation of PR interval, with a subsequent non-conducted P wave
Repeating 5:4 conduction ratio of P waves to QRS complexes
Relatively constant P-P interval despite irregularity of QRS complexes

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 Second degree AV block Mobitz type 2

Definition of Mobitz II block (Hay Block)

A form of 2nd degree AV block in which there is intermittent non-conducted P waves without progressive prolongation of the PR
interval
Other features:
The PR interval in the conducted beats remains constant
The P waves ‘march through’ at a constant rate
The 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, triple for two dropped beats, etc)
Clinical Significance
Mobitz II is much more likely than Mobitz I to be associated with haemodynamic compromise, severe bradycardia and progression
to 3rd degree heart block
Onset of haemodynamic instability may be sudden and unexpected, causing syncope (Stokes-Adams attacks) or sudden cardiac
death
The risk of asystole is around 35% per year
Mobitz II mandates immediate admission for cardiac monitoring, backup temporary pacing and ultimately insertion of a permanent
pacemaker

25
Mobitz Type 2

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 Complete heart block
ECG features-
PR interval irregular
Impulse created by SA node can’t cross AV node, thus QRS complex is not due to SA node and due to escape rhythm and it depends on
where the block is.
Complete AV block may occur at the level of the AV node or it may be infranodal, occurring below the AV node or anywhere in the His
bundle, bundle branches, and more distal conduction system.
P wave – 60-100/ min
QRS complex- 30-40/min
PP and RR interval are not same.
Ventricular rate depends on the site from where escape rhythm originates.
Junctional rhythm- 40-60 bpm if block is av nodal, QRS complex is narrow as impulse is carried through normal bundle pathway
If block is infra nodal then escape rhythm is produced by either bundle of his or ventricles, rate is 20-40 bpm, QRS complex is wide as impulse
transmitted through ventricular working myocardium.

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28
29
Complete heart block

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Most common symptom of conduction block is Syncope or pre syncope.
1 degree AV block: Pacemaker is not needed.
Pacemaker is used in:
Sick Sinus syndrome- ( rate 45-60 min)
Complete heart block or Complete AV dissociation( Rate <40/min)
Mobitz type 2 block( Rate < 15-20/Min)
Treatment in symptomatic Bradycardia Atropine1 mg Iv, Max dose=3 mg, If unresponsive then Transcutaneous Pacing)

Implantable Cadioverter Defibrillator reads ECG, Analyse ECG, Abnormal rhythm detection, DC shock delivery.
Indication of using ICD
Conditions that has tendency of developing Tachyarrhythmias
A- LV Aneurysm, Arrhythmogenic RV dysplasia.
B- Brugada syndrome
C- Cardiomyopathy of any etiology ( RCM/DCM/HOCM)

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 Shortened PR interval

•PR interval < 120ms

•Delta wave: slurring slow rise of initial portion of the QRS
•QRS prolongation > 110ms
•Discordant ST-segment and T-wave changes (i.e. in the opposite direction to the major
component of the QRS complex)
•Pseudo-infarction pattern in up to 70% of patients — due to negatively deflected delta waves in
inferior/anterior leads (“pseudo-Q waves”), or prominent R waves in V1-3 (mimicking posterior
infarction)

32
•Sinus rhythm with a very short PR interval (< 120 ms)
•Broad QRS complexes with a slurred upstroke to the QRS complex — the delta wave
•Dominant R wave in V1 suggests a left-sided AP, and is sometimes referred to as “Type A” WPW
•Tall R waves and inverted T waves in V1-3 mimicking right ventricular hypertrophy (RVH) — these changes are due to WPW and do
not indicate underlying RVH
•Negative delta wave in aVL simulating the Q waves of lateral infarction — this is referred to as the “pseudo-infarction” pattern
•Type A WPW

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•Sinus rhythm with very short PR interval (< 120 ms)
•Broad QRS complexes with a slurred upstroke to the QRS complexes — the delta wave
•Dominant S wave in V1 indicates a right-sided AP — sometimes referred to as “Type B” WPW
•Tall R waves and inverted T waves in the inferior leads and V4-6 mimic the appearance of left ventricular
hypertrophy (LVH) — again, this is due to WPW and does not indicate underlying LVH

34
right-sided AP (Type B WPW):
•Negative delta waves in leads III and aVF simulate the Q waves of prior inferior MI (= pseudo-infarction pattern)

35
Management of WPW:
DOC: Oral flecainide to prevent further episodes.
TOC: Radiofrequency ablation
Emergency Management: IV procainamide.

SVT

36
Symptoms:
Management of PSVT:
The leading symptom of most SVTs, in particular AV node
Acute:
re-entry and AV re-entry tachycardias, is rapid regular palpitations,
SBP<90 DC Shock
usually with abrupt onset and sudden termination,
SBP> 90
which can occur spontaneously or be precipitated by simple
Carotid sinus massage
movements. A common feature is termination by Valsalva
To prevent future episodes:
manoeuvres. In younger individuals with no structural heart
Oral verapamil
disease, the rapid heart rate can be the main pathological
Catheter ablation
finding.
In Children:
Irregular palpitations may be due to atrial premature beats,
PSVT Treatment:
atrial flutter with varying AV conduction block, atrial fibrillation
Face Ice pack
or multifocal atrial tachycardia. In patients with depressed
Valsalva maneuver
ventricular function, uncontrolled atrial fibrillation can reduce
Oculocardiac massage( Not recommended)
cardiac output and cause hypotension and congestive heart
Chemical cardioversion:
failure.
IV Adenosine 6 mg/12 mg, it increases AV nodal delay and decreases circus movement.
Other symptoms may include anxiety, dizziness, dyspnoea,
It causes bronchospasm so can’t be used in asthmatics.
neck pulsation, central chest pain and weakness.
Electrical cardioversion:
Polyuria may occur because of release of atrial natriuretic
Synchronised DC shock 120-200 joules
peptide in response to increased atrial pressures during the
AVNRT:
tachycardia, especially during AVNRT and atrial fibrillation.
1.Acute episode: SBP> 90
Prominent jugular venous pulsations due to atrial contractions
Carotid sinus massage
against closed atrioventricular valves may be observed
Adenosine
during AVNRT.
Synchronised DC Shock
Syncope has been reported in 10–15% of patients, usually
2. Crashing patient:
just after initiation of the arrhythmia or in association with
Synchronised DC Shock(120-200 joules)
a prolonged pause following its termination. It is more
3. Prevention of episodes of AVNRT
common if the patient is standing. However, in older patients
EPS(Electro physiological studies)
with concomitant heart disease, such as aortic stenosis,
Ablation of circuit
hypertrophic cardiomyopathy and cerebrovascular disease,
Verapamil
significant hypotension and syncope may result from moderately
Pulseless Ventricular Tachycardia:
fast ventricular rates.
Non Synchronized DC Shock 200J( given in ventricular fibrillation and pulseless VT)
Synchronised DC shock is given in all tachyarrhythmias, Atrial or ventricular.
Betablockers/AV blocking Stable Monomorphic VT-
IV Amiodarone/ IV procainamide.
agents are not to be given in SVT
produced due to WPW
syndrome- Guess why?
37
 RBBB Vs LBBB

Common in RBBB and LBBB QRS complex >120 ms ❖ In isolated RBBB there
isn’t RAD usually unless
2 points in RBBB there is bifascicular
block or RVH
1. rsR’,rR’,RR’ (M) pattern in V1 and W pattern in V6 (MARROW)
2. Septal q waves present and wide terminal S wave in V6
2 points in LBBB
1. QS, rS (W) pattern in V1 and RR’,R(M) pattern in V6 (WILLIAMS)
2. Septal q waves absent 38
 Bundle branch block

LBBB
•QRS duration > 120ms
•Dominant S wave in V1
•Broad monophasic R wave in lateral leads (I, aVL, V5-6)
•Absence of Q waves in lateral leads
•Prolonged R wave peak time > 60ms in leads V5-6 39
RBBB
•QRS duration > 120ms
•RSR’ pattern in V1-3 (“M-shaped” QRS complex)
•Wide, slurred S wave in lateral leads (I, aVL, V5-6)
40
 Ventricular premature complex

•Broad QRS complex (≥ 120 ms) with abnormal morphology

•Premature — i.e. occurs earlier than would be expected for the next sinus impulse
•Discordant ST segment and T wave changes.
•Usually followed by a full compensatory pause
•Retrograde capture of the atria may or may not occur
PVCs often occur in repeating patterns:
•Bigeminy — every other beat is a PVC
•Trigeminy — every third beat is a PVC
•Quadrigeminy — every fourth beat is a PVC
•Couplet — two consecutive PVCs
•NSVT — between three and thirty consecutive PVCs (see below)
Frequent or symptomatic PVCs may be due to:
•Anxiety
•Sympathomimetics
•Beta-agonists
•Excess caffeine
•Hypokalaemia
•Hypomagnesaemia
•Digoxin toxicity
•Myocardial ischemia

41
•Sinus rhythm with PVCs of two different morphologies (arrows)
•Note the appropriately discordant ST segments / T waves
•The pause surrounding the PVC is equal to double the preceding R-R interval (= a full compensatory pause)

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43
 Abnormalities in P wave

Right atrial enlargement produces a peaked P wave (P pulmonale) with amplitude:

•> 2.5 mm in the inferior leads (II, III and AVF)
•> 1.5 mm in V1 and V2
Also known as: Right Atrial Enlargement (RAE), Right atrial hypertrophy (RAH), right atrial abnormality

44
•Right atrial enlargement: P pulmonale
•P wave amplitude > 2.5mm in leads II, III and aVF

45
LAE produces a broad, bifid P wave in lead II (P mitrale) and enlarges the terminal negative portion of the P wave in V1.
In lead II
•Bifid P wave with > 40 ms between the two peaks
•Total P wave duration > 110 ms
In V1
•Biphasic P wave with terminal negative portion > 40 ms duration
•Biphasic P wave with terminal negative portion > 1mm deep

•Broad (>110ms), bifid P wave in lead II (P mitrale) with > 40ms between the peaks

46
P wave terminal portion > 40 ms duration in V1

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 LVH
It’s sufficient if you remember
•There are numerous voltage criteria for diagnosing LVH, summarised below only the Sokolov- lyon index
•The most commonly used are the Sokolov-Lyon criteria: S wave depth in V1 + tallest R and cantral index
wave height in V5-V6 > 35 mm
•Voltage criteria must be accompanied by non-voltage criteria to be considered diagnostic
of LVH
Voltage Criteria
Limb Leads
•R wave in lead I + S wave in lead III > 25 mm
•R wave in aVL > 11 mm
•R wave in aVF > 20 mm
•S wave in aVR > 14 mm
Precordial Leads
•R wave in V4, V5 or V6 > 26 mm
•R wave in V5 or V6 plus S wave in V1 > 35 mm
•Largest R wave plus largest S wave in precordial leads > 45 mm
Non Voltage Criteria
•Increased R wave peak time > 50 ms in leads V5 or V6
•ST segment depression and T wave inversion in the left-sided leads: AKA the left
ventricular ‘strain’ pattern
48
LVH by voltage criteria: S wave in V2 + R wave in V5 > 35 mm

LV strain pattern: ST depression and T wave inversion in the lateral leads

49
Left ventricular hypertrophy (LVH):
•Markedly increased LV voltages: huge precordial R and S waves that overlap with the adjacent leads (SV2 + RV6 >> 35 mm).
•R-wave peak time > 50 ms in V5-6 with associated QRS broadening.
•LV strain pattern with ST depression and T-wave inversions in I, aVL and V5-6.
•ST elevation in V1-3.
•Prominent U waves in V1-3.
•Left axis deviation.
Severe LVH such as this appears almost identical to left bundle branch block — the main clue to the presence of LVH is the excessively high LV voltages.
50
 RVH
It’s sufficient if you remember
Diagnostic criteria: that in RVH there will be RAD
Right axis deviation of +110° or more. and R/S>1 in V1
Dominant R wave in V1 (> 7mm tall or R/S ratio > 1).
Dominant S wave in V5 or V6 (> 7mm deep or R/S ratio < 1).
QRS duration < 120ms (i.e. changes not due to RBBB).
Supporting criteria:
Right atrial enlargement (P pulmonale).
Right ventricular strain pattern = ST depression / T wave inversion in the right precordial (V1-4) and inferior (II, III, aVF) leads.
S1 S2 S3 pattern = far right axis deviation with dominant S waves in leads I, II and III.
Deep S waves in the lateral leads (I, aVL, V5-V6).
Other abnormalities caused by RVH
Right bundle branch block (complete or incomplete).

ECG Pearl
There are no universally accepted criteria for diagnosing RVH in the presence of RBBB; the standard voltage criteria do not apply.
However, the presence of incomplete / complete RBBB with a tall R wave in V1, right axis deviation of +110° or more and supporting
criteria (such as RV strain pattern or P pulmonale) would be considered suggestive of RVH.
Causes:
Pulmonary hypertension
Mitral stenosis
Pulmonary embolism
Chronic lung disease (cor pulmonale)
Congenital heart disease (e.g. Tetralogy of Fallot, pulmonary stenosis)
Arrhythmogenic right ventricular cardiomyopathy

51
Typical appearance of RVH:
Right axis deviation (+150 degrees).
Dominant R wave in V1 (> 7 mm tall; R/S ratio > 1)
Dominant S wave in V6 (> 7 mm deep; R/S ratio < 1).
Right ventricular strain pattern with ST depression and T-wave inversion in V1-4.

52
Right axis deviation (+150 degrees)
P pulmonale (P wave in lead II > 2.5 mm)
Incomplete RBBB
Right ventricular strain pattern with T-wave inversion and ST depression in the right precordial (V1-3) and inferior
(II, III, aVF) leads.
53
 Acute Coronary Syndrome

ST elevation >1 mm in any two or more adjacent precordial or limb leads. ST elevation is measured at the J point. The J point is the junction
between the terminal portion of the QRS complex and beginning of the ST segment. The preceding T-P segment serves as baseline for measuring
the ST elevation. The PR interval is used if the T-P segment is too short or is obscured by a U wave or a P wave of sinus tachycardia.

A,B,C,D are due to ACS, F due to Acute

pericarditis (Concave upward ST
elevation, rarely it may be due to MI)

Sequential ST-T changes in MI

54
Causes of ST elevation other than STEMI:
■ Normal elevation of the ST segment at the transition zone
■ Early repolarization
■ LBBB
■ Left ventricular hypertrophy (LVH)
■ Acute pericarditis(Diffuse ST elevation without reciprocal changes)
■ Left ventricular aneurysm
■ Electrolyte abnormalities: hyperkalemia and hypercalcemia
■ Wolff-Parkinson-White (WPW) syndrome
■ Osborn wave of hypothermia
■ Brugada ECG
■ Others: Pacemaker rhythm, ectopic ventricular complexes, Takotsubo cardiomyopathy, tumors or
trauma involving the ventricle
Hypothermia can Cause J point elevation.
In STEMI there will be ST elevation along with reciprocal ST depression in the opposite leads.

Causes of ST Depression Inverted T waves

❑ Myocardial ischaemia / NSTEMI Inverted T waves are seen in the following conditions:
❑ Reciprocal change in STEMI Posterior MI ❑ Normal finding in children
❑ Digoxin effect ❑ Persistent juvenile T wave pattern
❑ Hypokalaemia ❑ Myocardial ischaemia and infarction (including Wellens Syndrome)
❑ Supraventricular tachycardia ❑ Bundle branch block
❑ Right bundle branch block ❑ Ventricular hypertrophy (‘strain’ patterns)
❑ Right ventricular hypertrophy ❑ Pulmonary embolism
❑ Left bundle branch block ❑ Hypertrophic cardiomyopathy
❑ Left ventricular hypertrophy ❑ Raised intracranial pressure
❑ Ventricular paced rhythm ❑ ** T wave inversion in lead III is a normal variant. New T-wave inversion
(compared with prior ECGs) is always abnormal. Pathological T wave
inversion is usually symmetrical and deep (>3mm

55
 Localisation of Infarction
❑ Inferior leads- Lead 2,3, avF ✓ ST elevation in lead 1,avL, V1-V6 – Extensive
❑ Septal leads- V1(mainly),V2 anterior wall MI(Infarction in anterior, septal and
❑ Anterior leads- V2,V3,V4 lateral wall.
❑ Lateral leads- V5,V6 ✓ ST elevation in V1-V4- Antero septal MI
❑ High lateral leads- Lead 1, ✓ ST elevation in V3-V6 – Antero lateral MI
avL ✓ ST depression and tall R waves in V1-V4- Posterior
wall MI
✓ ST elevation in V5,V6- Lateral wall involvement if
elevated in Lead 1 and avL too then high lateral
wall is also involved.

56
❑ Right coronary artery supplies- Inferior wall(in Right
dominant people), right ventricle, posterior wall
❑ Left coronary artery supplies- Septum, lateral wall,
anterior wall.
❑ Septum and anterior wall is supplied purely by
LAD(branch of LCA) by S1 and D2.( see figure on
the left).
❑ Lateral wall and high lateral wall may be supplied
by LCx or LAD( both are branches of LMCA).
❑ SA node is supplied by RCA.
❑ Inferior wall is supplied by Posterior descending
artery which arises from RCA( In Right dominant
person) or from LCx( in left dominant persons).
Majority people are right dominant.
❑ So, inferior wall MI(diagnosed as ST elevation in
Lead 2,3,avF) is mostly due to RCA occlusion and
may be due to LCx occlusion if it is of left dominant
person.
❑ Anterior and septal MI( Diagnosed by ST elevation
in V1-V4) is always due to LAD occlusion as
supplied purely by LAD.
❑ Lateral and high lateral MI(Diagnosed by ST
elevation in lead 1,avL and V5,V6) may be due to
LAD or LCx.

57
58
Extensive Anterior STEMI (acute):
ST elevation in V1-6 plus I and aVL (most marked in V2-4)
Minimal reciprocal ST depression in III and aVF
Q waves in V1-2, reduced R wave height (a Q-wave equivalent) in V3-4
Most probably due to LAD occlusion before D1.
Why not its due to LCx?
As though lateral and high lateral wall MI may occur due to occlusion of LCx but here there is anterior wall and septum involvement
which occurs purely due to LAD occlusion so its due to LAD occlusion.
59
Extensive anterior MI (“tombstoning” pattern)
Massive ST elevation with “tombstone” morphology is present throughout the precordial (V1-6) and high lateral leads (I, aVL)
This pattern is seen in proximal LAD occlusion and indicates a large territory infarction with a poor LV ejection fraction and high likelihood of
cardiogenic shock and death

60
Acute anteroseptal STEMI with STE maximal in V1-4.
Due to LAD occlusion.
Lateral wall is spared guess why?
Remember lateral wall can also be supplied by LCx so here its spared as its supplied by Lcx.

61
Early inferior STEMI:
Hyperacute (peaked) T waves in II, III and aVF with relative loss of R wave height
Early ST elevation and Q-wave formation in lead III
Reciprocal ST depression and T wave inversion in aVL( Its very important in the setting of INF wall MI as Lead avL is just opposite to the inferior surface and lead 3 so reciprocal
changes are seen in this lead)
ST elevation in lead III > lead II suggests an RCA occlusion; the subtle ST elevation in V4R would be consistent with this.
Note how the ST segment morphology in aVL is an exact mirror image of lead III. The concept of reciprocal change can be further highlighted by taking lead aVL and inverting it.
Notice how the ST morphology now looks identical to lead III:

62
Inferior STEMI:
Marked ST elevation in II, III and aVF with early Q-wave formation.
Reciprocal changes in aVL.
ST elevation in lead III > II with reciprocal change present in lead I and ST elevation in V1-2 suggests RCA occlusion with associated RV infarction:
This patient should have right-sided leads to confirm this.

63
 Bradycardia and AV Block in inferior STEMI
Up to 20% of patients with inferior STEMI will develop either second- or third-degree AV block. There are two presumed mechanisms for this:
❑ Ischaemia of the AV node due to impaired blood flow via the AV nodal artery. This artery arises from the RCA 80% of the time, hence its involvement in inferior STEMI due to RCA
occlusion.
❑ Bezold-Jarisch reflex = increased vagal tone secondary to ischemia.( Block can be 1, 2 degree or Complete, There is an ecg of the same in our dept)

Inferior STEMI with third degree heart block and slow junctional escape rhythm.

64
 How to recognize a lateral STEMI
ST elevation in the lateral leads (I, aVL, V5-6).
Reciprocal ST depression in the inferior leads (III and aVF).
ST elevation primarily localized to leads I and aVL is referred to as a high lateral STEMI.

High Lateral STEMI:

ST elevation is present in the high lateral leads (I and aVL).
There is reciprocal ST depression in the inferior leads (III and aVF).
65
 A 29 Year old Male presented With history of presyncope(Sudden blackouts
while standing up from sitting posture), Coincidentally during checking his
spO2 in pulse oximeter his friend found that he is having a pulse of 46/min,
He went to a young MBBS practitioner, the doctor ordered an ECG and
then prescribed beta agonist and told him to have Tea, being not satisfied
he went to a cardiologist and the Cardiologist again ordered an ECG with
long lead 2. The ECG is as follows, What is your diagnosis and what is the
Management?

Complete heart block

66
 Practice ECGs

Complete heart block with STEMI

67
Rhythm- Sinus, Regular
Rate- 135 bpm
Right axis deviation
PR interval normal
Positive QRS Complex {with upright P waves} in avR
Lead 1: Inversion of all complexes, aka Global negativity (inverted P wave, negative qrs complexes, inverted T wave)
Absent R wave progression in the chest leads( Dominant S waves throughout)
Lead 1+Lead 3= Lead 2 maintained so no inversion of leads
Probably this is a case of dextrocardia with Sinus arrhythmia
A
68
Rhythm- Sinus, Regular
Rate- 75 bpm
Axis- Normal
PR interval normal
T wave inversion in V1-V4, Biphasic T in V5
Differential diagnosis of T wave inversion (see page 55)
69 B
Rhythm- Regular, sinus
Rate- 71 bpm
Axis- LAD
PR interval- Normal
T wave inversion in V3,V4,V5,V6, 1 and aVL
Probably due ischemic changes
70
C
Rhythm- Sinus, regular
Rate- Normal
Axis- Normal
•Sinus rhythm with very short PR interval (< 120 ms)
•Broad QRS complexes with a slurred upstroke to the QRS complexes — the delta wave
•Dominant S wave in V1 indicates a right-sided AP — sometimes referred to as “Type B” WPW D
•Tall R waves and inverted T waves in the inferior leads and V4-6 mimic the appearance of left ventricular hypertrophy (LVH) — again, this is due to WPW and does not
indicate underlying LVH 71
Rhythm- Regular, non sinus
Rate- 60 bpm
Axis- Normal
PR interval not equal to RR interval.
No coordination between atrial and ventricular activity.
Narrow QRS complex
Probably complete AV dissociation, in Junctional rhythm.

72
E
Rhythm- Sinus, regular
Rate- 38 bpm
Axis- Left axis deviation
P wave normal
PR interval normal
Septal q wave absent in chest leads
Prominent S wave in V1, V2 and RR’ Pattern in V5, V6.
S wave in V1+R in V6> 35 mm
So, probably this is a case of sinus bradycardia associated with LVH with complete LBBB morphology
73 F
Rhythm- Irregularly irregular
Ventricular Rate- 130 bpm, atrial rate- 375 bpm
Axis- Normal axis
P wave absent
QRS complex interval irregularly irregular.
Fibrillatory wave present in V1
So, Probably this is a case of Atrial fibrillation.

G
74
Rhythm- Regular, Sinus
Rate- 83 bpm
Axis- Left axis deviation
P wave normal
PR interval Normal
ST elevation in V1, V2,V3, V4, V5, V6
Presence of q waves in V1-4
So, Probably this is a case of ST elevation MI in anterolateral wall and septum, i.e., Extensive anterior wall MI

75 H
Rhythm- Regular, Sinus rhythm
Rate- 83 bpm
Axis- RAD
Bifid P wave
PR interval > 200 ms
Positive R wave in V1, R wave peak time in V1>.05s
Slurred S wave in V5,6
Secondary T Wave inversion in V1-3, primary t inversion in v4-6
Complete RBBB pattern
I
So, probably this is a case of complete RBBB with PR prolongation 76
Rhythm- Regular, Non Sinus
Rate- 65 bpm
Absent P wave
ST elevation in lead 2, 3, aVF
Reciprocal changes in Lead 1, aVL, V2, V3, V4
So, Probably this is a case of inferior wall MI with accelerated junctional rhythm

J77
Rhythm- Regular, Sinus
Rate- 55 bpm
Axis- Normal
P wave normal
PR interval normal
J point elevation in lead 2, 3, aVF, V3, V4, V5, V6, Concave upward pattern
So, Probably this is a case of Early repolarisation.
K
78
Rhythm- Regular,
Rate- 88 bpm
Axis-Normal
P wave abnormal,
ST elevation in V1, V2, V3, V4 with reciprocal changes.
Q waves in V1-4
ST elevation in lead 2,3, avF
So, probably this is a case of Anteroseptal MI and a developing inferior wall MI L
79
Rhythm- Normal
Rate-69 bpm
Axis- LAD
P wave normal,
PR interval normal,
J point elevation in V2, V3, V4
So, probably this is a case of Early Repolarisation

M
80
Rhythm- Irregular, Sinus
Rate- 125 bpm
Axis- Normal
R/S ratio>1 in V1 and T wave inversion V1,2,3 probably normal variation as this remains up to 10 years of age and this child is
of 1 year.
P wave, PR interval normal
T wave inversion in V1, V2, V3.
So, This is a case of sinus Arrhythmia
N
81
Rhythm-Sinus
Rate- 80 bpm
Axis- LAD
rSR’ pattern in V1,qrS pattern in V6 with slurred S wave and septal Q preserved in V6, R wave peak time in V1>.05s, so RBBB
pattern.
Broad QRS so complete RBBB pattern.
Premature ventricular complexes are there.
So, this is a case of RBBB with LAD probably due to bifascicular block. O
82
Rate- 83 bpm
Rhythm- Regular
Axis- Normal
PR prolongation
QRS complex are wide with rS pattern in V1 and monophasic R with absence of septal q waves in V6.
R wave peak time in V6 is more than .5s P
So, probably this is an ECG of LBBB. 83
Rate- 69 bpm
Rhythm- Regular, Sinus
Axis- Normal
T wave inversion in lead 1, avL, V6
V1-V3 J point elevation.

84 Q
Rhythm- Regular
Rate- 166 bpm
Axis- LAD
Absent p waves
Wide QRS Complex
So, This is a case of wide complex tachycardia.

R85
Rate- 83 bpm
Rhythm- Sinus, regular
Axis- Normal
Sinus rhythm with very short PR interval (< 120 ms)
Broad QRS complexes with a slurred upstroke to the QRS complexes — the delta wave
Dominant S wave in V1 indicates a right-sided AP — sometimes referred to as “Type B” WPW
Tall R waves and inverted T waves in the inferior leads and V4-6 mimic the appearance of left ventricular hypertrophy (LVH) — again, this is due to WPW
and does not indicate underlying LVH
86 S
Rate-42 bpm
Rhythm- regular
Axis- Normal
P waves are normal
Rhythm strip shows block of every second P wave, 2:1 block(For every 2 P waves 1 is conducted)
QRS complex are wide and have RBBB morphology.

T
87
Ventricular Rate- 110 bpm, Atrial rate- 375 bpm
Rhythm- Irregular
Axis-Normal
Absence of P wave instead fibrillatory waves are present in V1.
QRS complex <120 ms.
So, this is an ECG of Atrial fibrillation

88 U
Rate-57 bpm
Rhythm- Regular, Non sinus
Axis- LAD
Wide qS complex in lead 2,3, avF with J point elevation.
Complete asynchrony between P wave and Qrs complex, both are independent to each other, P waves overlapping with qrs complex
sometimes.
PP interval not equal to RR interval.
Most probably this is an ecg of Inferior wall MI with Complete AV dissociation.
89
Rate- 60 bpm
Rhythm- Irregular
Axis-Normal
Supraventricular ectopic is seen in the form of inverted P waves in lead 2, following in he pattern of 2:1
So, this is an ECG of Supraventricular bigeminy

90
Rate-65 bpm
Rhythm- regular, sinus
Axis-LAD
T inversion in Lead 1,aVL and V5,6
Differential diagnosis of T wave inversion(see page 55)

91
Rate- 60
Rhythm- Regular
Axis- Normal
Wide QRS complex with LBBB pattern( rS wave in V1,2 and RR’ pattern in V5 with absence of septal q in V5,6)
LVH according to Sokolow lyon index
So, this is an ECG of Complete LBBB with discordant ST-T changes in chest leads with LVH

92
Rate-83 bpm
Rhythm- Regular
Axis- Left ward axis
rsR’ pattern in V1, R wave peak time in V1 is more than .05 s. septal q wave present in V6 and slurred s waves in V6.
So, probably this is an ecg of RBBB

93
Rate-61 bpm
Rhythm- Regular
Lead 1+ Lead 3 not equal to lead 2
Normal R wave progression in chest leads
So, this is an ECG of inversion of limb leads.

94
FAQs
1. What are the types of leads?
2. How to calculate rate and rhythm?
3. How to calculate axis in a ECG?
4. What are the causes of LAD,RAD?
5. What are the normal waves in an ECG paper?
6. What does each wave in an ECG signifies?
7. What are the normal duration of PR interval, QRS complex, QT interval?
8. What are the P wave abnormalities?
9. What does increased PR interval suggest?
10.What is corrected QT interval? Why it is corrected?
11.When you will call a QRS complex as broad?
12.What is preexcitation syndromes?
13.How to diagnose LVH, RVH?
14.What is Einthoven law?
15.Which are the anterior leads, Septal leads, Lateral leads, Inferior leads, high lateral leads?
16.What are causes of ST elevation?
17.What are the causes of ST depression?
18.What is tachycardia?
19.What is bradycardia?
20.How to calculate the rate if the rhythm is irregularly irregular?
21.Which conditions causes irregularly irregular RR interval and which causes regularly irregular RR interval?
22.Management of SVT, MI, Blocks.
23.Side effects of important drugs.
24.Localization of infarct and localization of the occlusion in the artery.

95
Resources
➢ Dr Najeeb's videos of ECG
➢ ECG videos of Marrow
➢ ECG videos of Dr Marwah
➢ Basic and Bedside Electrocardiography by Romulo F. Baltazar,MD, FACC
➢ Kumar and clark’s Clinical Medicine(for management of conditions only)
➢ LITFL website

If you find any discrepancy here please let me know in my WhatsApp no- 7679657287
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