Electrocardiography (ECG) TAN DI-SHEN 2021 The standard ECG has 12 leads:

Introduction to ECG: -3 standard limb leads

-ECG is a representative of electrical events of the cardiac cycle -3 augmented limb leads
-Each event has a distinctive waveform, ECG is the study of waveform which can lead to greater -6 precordial leads
insight into a patient’s cardiac pathophysiology
-There are several possible pathologies we can identify with the help of ECG:
1. Arrhythmias
2. Myocardial ischemia and infarction
3. Pericarditis
4. Chamber hypertrophy
5. Electrolyte disturbances (eg. hypokalemia, hyperkalemia)
6. Drug toxicity (eg. digoxin and several drugs that prolong the QT interval)
-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

Pacemakers of the heart:

1. SA node: Dominant pacemaker with an intrinsic rate of 60-100 beats/minute
2. AV node: Back-up pacemaker with an intrinsic rate of 40-60 beats/minute
3. Ventricular cells: Back-up pacemaker with an intrinsic rate of 20-45 beats/minute

Yellow: 6 standard leads

Red: 6 chest leads
Green: The rhythm strip used for determining heart rate

P wave- Atrial depolarization

QRS wave- Ventricular depolarization
T wave- Ventricular repolarization

ECG leads:

The QRS complex should be dominantly upright in leads I and II

QRS and T waves tend to have the same general direction in the limb leads

5
10 rules of normal ECG by Professor Chamberlains
1

All waves are negative in lead aVR

PR interval should be 120-200ms or 3-5 little squares

The R wave must grow from V1 to at least V4

The S wave must grow from V1 to at least V3 and disappear in V6
The width of QRS complex should not exceed 110ms, less than 3 little squares
 7 2. Determine regularity
3. Assess the P waves
4. Determine PR interval
5. Determine QRS duration

Calculating rate -Heart rate =

300
𝑅−𝑅 𝑖𝑛𝑡𝑒𝑟𝑣𝑎𝑙 (𝑙𝑎𝑟𝑔𝑒 𝑠𝑞𝑢𝑎𝑟𝑒𝑠)

The ST segment should start isoelectric except in V1 and V2 where it may be

elevated

Determine regularity

-Look at R-R interval (using a caliper or markings on a pen

or paper)
-Regular (are they equidistant apart)? Occasionally
irregular? Regularly irregular? Or Irregularly irregular?
The P waves should be upright in I, II and V2 to V6
Assess the P waves -Are there P waves?
9 -Do the P waves all look alike?
-Do the P waves occur at a regular rate?
-Is there one P wave before each QRS?

Determine PR interval and

QRS duration

There should be no Q wave or only small q less than 0.04 seconds in width in I, II,
V2 to V6

10

Rhythm summary

The T wave must be upright in I, II, V2 to V6 Rate: 90-95 bpm

Regularity: regular
Rhythm analysis P waves: normal
PR interval: 0.12s
5 steps
QRS duration: 0.08s
1. Calculate rate Interpretation: Normal sinus rhythm

Examples of abnormal rhythm Example 1: QRS duration: 0.08s (7th wide)

Interpretation: NSR with 1 premature ventricular contraction

Rate: 30bpm Supraventricular arrhythmia

Regularity: regular Example 5:
P waves: normal
PR interval: 0.12s
QRS duration: 0.10s
Interpretation: Sinus bradycardia Rate: 100bpm
Management: No intervention needed if asymptomatic. If Regularity: irregularly irregular
symptomatic, consider pacemaker insertion P waves: none
PR interval: none
QRS duration: 0.06s
Example 2: Interpretation: Atrial fibrillation
-No organized atrial depolarization, so no normal P waves
(impulses are not originating from SA node)
-Atrial activity is chaotic (resulting in irregularly irregular
Rate: 130bpm rate)
Regularity: regular
P waves: normal
PR interval: 0.16s Example 6:
QRS duration: 0.08s
Interpretation: Sinus tachycardia

Rate: 70bpm
Premature beats Regularity: regular
Example 3: P waves: flutter waves
PR interval: none
QRS duration: 0.06s
Interpretation: Atrial flutter
Rate: 70bpm -Rapid atrial rate: “saw-tooth appearance”
Regularity: Occasionally irregular -May have high atrial rate and AV blocks occur as it cannot
P waves: 2/7 different contour keep up with high atrial rate. Most commonly 2:1 block. The
PR interval: 0.14s (except 2/7) ventricular rate may be high.
QRS duration: 0.08s
Interpretation: NSR with premature atrial contraction Example 7:

Example 4:
Rate: 74 -> 148 bpm
Regularity: Regular -> regular
P waves: Normal -> none
Rate: 60bpm PR interval: 0.16s -> none
Regularity: Occasionally irregular QRS duration: 0.08s
P waves: none for 7th QRS Interpretation: Paroxysmal supraventricular tachycardia
PR interval: 0.14s (PSVT)
 -The heart rate suddenly speeds up and the P waves are lost PR 120-200 Heart blocks (drugs, electrolytes)

QRS 80-120 Conduction abnormalities (bundle branch

Ventricular arrhythmias block)
Example 8:
QT Varies with heart rate, Repolarization abnormalities, ion
>450 can lead to channelopathies (Prolonged QT syndrome)
ventricular tachycardia
Rate: 160 bpm
Regularity: regular The QRS Axis
P waves: none
PR interval: none Introduction -It represents overall direction of the heart’s electrical activity
QRS duration: wide (>0.12sec) -Abnormalities hint at:
Interpretation: Ventricular tachycardia 1. Ventricular enlargement
-Impulse is originating in the ventricles (no P waves, wide 2. Conduction blocks (eg. hemiblocks)
QRS)
The Axis

Example 9:

Rate: none
Regularity: irregular irregular
P waves: none
PR interval: none
QRS duration: wide, if recognizable 1. Normal axis from -30° to +90°
Interpretation: Ventricular fibrillation 2. -30° to -90° is referred to as a left axis deviation (LAD)
-Chaotic rhythm of ventricular fibrillation without clearly 3. +90° to +180° is referred to as a right axis deviation (RAD)
discernible P waves, QRS complexes or T waves
The quadrant approach 1. QRS complex in lead I and aVF
2. Determine if they are predominantly positive or negative
Normal ranges for ECG intervals:
3. The combination should place the axis into one of the 4
quadrants below

-When LAD is present, look at the QRS in lead II. If it is positive,

Interval Normal range (per ms) Possible pathology

the LAD is non-pathologic or the axis is normal. If negative, it is

pathologic

Example 1:

Negative in I, positive in aVF -> Right axis deviation (RAD)

Example 2:

Example 1:

Positive in I, negative in aVF -> Predominantly positive in II ->

Normal axis (non-pathologic LAD)

The equiphasic 1. Most equiphasic QRS complex QRS axis= -30°

approach 2. Identified Lead lies 90° away from the Lead
3. QRS in this second lead is positive or negative Example 2:
 -Best seen in Lead II

P wave completely -Atrial fibrillation

absent -Prolonged period of sinus arrest or SA block
QRS axis= +90° -Hyperkalemia

Causes of LAD -Left ventricular hypertrophy P wave intermittently -Sinus arrest or SA block (intermittent)
-Left anterior fascicular block (due to fibrosis of conducting system) absent
-Inferior myocardial infarction (QRS axis is directed away from
P wave inverted -Electrode misplacement
infarcted areas)
-Dextrocardia
-Ventricular tachycardia (When VT arises from a focus in the left
-Ectopic atrial rhythm
ventricular apex, the wave of depolarization spreads out through the
rest of the myocardium from that point, resulting in left axis Tall P wave -Normal P wave < 2.5 small squares in amplitude
deviation) -It is known as Pointed P wave (P Pulmonale), is often due to
-Wolff–Parkinson–White (WPW) syndrome pulmonary disorders
Causes of RAD -Right ventricular hypertrophy
-WPW syndrome (left-sided accessory pathway)
-Anterolateral myocardial infarction (QRS axis is directed away
from infarcted areas)
-Dextrocardia
-Left posterior fascicular block
Example:
P wave
Introduction -It indicates atrial depolarization
-It is always positive in Lead I and II
-It is always negative in lead aVR
-Tall P waves (3.5 mm in lead II)

Wide P wave -Normal P wave <3 small squares in duration

-Left atrial enlargement-broad, bifid P waves- referred to as ‘P
mitrale’
-Because left atrial enlargement is a result of mitral valve disease.
-The P wave becomes broad because the enlarged left atrium takes
-< 3 small squares in duration longer than normal to depolarize
-< 2.5 small squares in amplitude
-Commonly biphasic in Lead V1

Introduction -It is a negative deflection that precedes R wave

-It also represents the normal left-to-right depolarization of the
interventricular septum
-Q waves are usually absent from most of the leads. Small Q waves
are normal in leads that look at the heart from the left: I, II, aVL, V5
and V6. It is known as small “septal” Q wave

PR interval
Introduction -The time taken for the depolarization wave to pass to from its origin
in the SA node, across the atria, and through the AV node into
ventricular muscle
-Its calculated from the start of P wave to to start of QRS complex
-Normal range: 120-200msec (3-5 small squares) Q waves in different -Small Q waves are normal in most leads
leads -Deeper Q waves (>2 mm) may be seen in leads III and aVR as a
Short PR interval -Wolff–Parkinson–White (WPW) syndrome (Additional connection
normal variant
between the atria and the ventricles (an accessory pathway) that
-Under normal circumstances, Q waves are not seen in the
conducts more quickly than the AV node, with presence of delta
right-sided leads (V1-3)
wave that indicates ventricular pre-excitation.)
Pathological Q waves Presence of either one
-Lown–Ganong–Levine (LGL) syndrome (the accessory pathway in ->2 small squares deep
LGL syndrome does not activate the ventricular muscle directly. ->1 small square wide
Instead, it simply connects the atria to the bundle of His. As a result, -> 25% of depth of QRS complex
the AV node is bypassed (so the PR interval is short) but there is no -Seen in leads V1-3
ventricular pre-excitation (and therefore there is no delta wave))
Causes of pathological -Myocardial infarction (Q waves start to appear within a few hours
-AV nodal escape rhythm, AV ectopics, AV reentry tachycardia Q waves of the onset of STEMI and 90 % become permanent)
-Cardiomyopathies (hypertrophic HCM, infiltrative myocardial
-Accelerated AV nodal conduction (the presence of a short PR disease)
interval in isolation, with no history of re-entry tachycardia) -Lead placement errors (eg. upper limbs placed on lower limbs)

Long PR interval -First degree heart block Absent Q waves -The absence of small septal Q waves in leads V5-6 should be
considered abnormal, and its most commonly due to LBBB

Examples of Example 1:
pathological Q waves

Q waves
 QRS complex
Introduction -It indicates ventricular depolarisation
-Normal QRS width is 70-100 ms (a duration of 110 ms is sometimes
observed in healthy subjects). The QRS width is useful in
determining the origin of each QRS complex (e.g. sinus, atrial,
junctional or ventricular)
-Narrow complexes (QRS < 100 ms) are supraventricular in origin
-Broad complexes (QRS > 100 ms) may be either ventricular in
origin, or due to aberrant conduction of supraventricular complexes
(e.g. due to bundle branch block, hyperkalaemia or sodium-channel
blockade)

Inferior Q waves (II, III, aVF) with ST elevation due to acute MI

Example 2:

Narrow QRS complex -Narrow (supraventricular) complexes arise from three main places:
1. Sino-atrial node (= normal P wave)
2. Atria (= abnormal P wave/ flutter wave/ fibrillatory wave)
3. AV node / junction (= either no P wave or an abnormal P
Inferior Q waves (II, III, aVF) with T-wave inversion due to wave with a PR interval < 120 ms)
previous MI -Common cause is supraventricular tachycardia

Example 1:
Example 3:

Normal sinus rhythm with narrow QRS complex

Example 2:

Lateral Q waves (I, aVL) with ST elevation due to acute MI

with broad, notched R waves and absent Q waves in the

lateral leads.
3. Hyperkalemia is associated with a range of abnormalities
including peaked T waves
4. Wolff-Parkinson White syndrome is characterised by a short
PR interval and delta waves

Narrow QRS complexes are associated with regular flutter waves. R waves
(Atrial flutter)
Introduction -The R wave is the first upward deflection after the P wave. The R
wave represents early ventricular depolarisation
Example 3: -Right-sided leads (V1): negative
-Left-sided leads (V6): positive

Narrow QRS complexes with no visible P waves. (Junctional

tachycardia)

Broad/ wide QRS -A QRS duration >100 ms is abnormal

complex -A QRS duration >120 ms is required for the diagnosis of bundle
branch block or ventricular rhythm

Causes are:
-Bundle branch block (RBBB or LBBB) -Abnormalities R wave:
-Hyperkalaemia 1. Dominant R wave in V1
-Pre-excitation (eg. Wolff-Parkinson-White syndrome) 2. Dominant R wave in aVR
-Ventricular tachycardia 3. Poor R wave progression

Dominant/ tall R wave -It is normal in children and young adults

Example 1:
in V1 Causes:
-Right ventricular hypertrophy
-Right bundle branch block (RBBB)
-Wolff-Parkinson-White (WPW) type A
-Posterior myocardial infarction

Example 1:
Broad QRS complexes with no visible P waves (Ventricular
tachycardia)

Many causes of broad QRS can be identified by pattern recognition:

1. Right bundle branch block produces an RSR’ pattern in V1
and deep slurred S waves in the lateral leads.
2. Left bundle branch block produces a dominant S wave in V1
 Normal paediatric ECG (2 years old) Presence of poor R wave progression

Example 2: ST segment
Introduction -It is a transient period with no electrical activities passed through
the myocardium
-It is measured from the end of S to the beginning of the T wave

Right ventricular hypertrophy (RVH)

Dominant R wave in Causes:

aVR -Poisoning with sodium-channel blocking drugs (e.g. TCAs)
-Dextrocardia
-Incorrect lead placement (left/right arm leads reversed)
-Commonly elevated in ventricular tachycardia (VT) -It is isoelectric and lies at the same level as the ECG’s baseline
Poor R wave -Ideally, moving from V1 to V6, R wave should be gradually -The most important cause of ST segment abnormality (elevation or
progression increasing while the S wave should be gradually decreasing. depression) is myocardial ischaemia or infarction
Eventually, R wave and S wave should be equal at transition point ST segment elevation -Causes of ST segment elevation:
which is which is between V3 and V4 1. Acute myocardial infarction
-It is described with an R wave ≤ 3 mm inV3 and is caused by: 2. Pericarditis
1. Prior anteroseptal myocardial infarction 3. Left bundle branch block (LBBB)
2. Left ventricular hypertrophy or Right ventricular hypertrophy 4. Coronary vasospasm (Prinzmetal's angina): Very similar and
(If the R:S in V2 then its more towards RVH, if R:S in V5 indistinguishable from STEMI. ECG changes are transient
then its moving towards LVH) and reversible with vasodilators
5. Ventricular aneurysm
Example 1: 6. Brugada syndrome

Morphology of ST elevation in MI:

Inferior STEMI (There is ST segment elevation in leads II, III and

aVF, with ‘reciprocal’ ST segment depression in leads I and aVL)
Morphology of ST elevation in other conditions:
Example 2:

Anterior STEMI (ST elevation in V1-V4)

Example 3:

Example 1:

Concave “saddleback” ST elevation in leads I, II, III, aVF, V5-6 with

depressed PR segments. There is reciprocal ST depression and PR
elevation in leads aVR and V1 (Pericarditis)

ST segment depression -Causes of ST segment depression:

1. Myocardial ischaemia/ NSTEMI
 2. Reciprocal change in STEMI
3. Posterior MI
4. Digoxin effect
5. Hypokalaemia
6. Supraventricular tachycardia
7. Right bundle branch block (RBBB)
8. Right ventricular hypertrophy

ST elevation at Lead II, III and aVF, meantime there’s reciprocal

changes of ST depression at Lead aVL

Example 3:

Morphology of ST depression in myocardial ischaemia:

Acute posterior STEMI causes ST depression in the anterior leads

V1-3, along with dominant R waves (“Q-wave equivalent”) and
upright T waves. There is ST elevation in the posterior leads V7-9
Example 1:
T waves
Introduction -It indicates ventricular repolarization

-Normal characteristics of T waves:

1. Upright in all leads except aVR and V1
2. Amplitude < 5mm in limb leads, < 10mm in precordial leads
(10mm males, 8mm females)
3. Duration relates to QT interval

-T wave abnormalities:
ST depression in Lead I, II, aVL and V4-6 that indicates myocardial 1. Peaked T waves
ischemia 2. Hyperacute T waves
3. Inverted T waves
4. Biphasic T waves
Example 2:

5. ‘Camel Hump’ T waves Hyperacute T waves

6. Flattened T waves

Peaked T waves

Tall, narrow, symmetrically peaked T-waves are characteristically

seen in hyperkalemia

Example 1:
Broad, asymmetrically peaked or ‘hyperacute’ T-waves (HATW) are
seen in the early stages of ST-elevation MI (STEMI), and often
precede the appearance of ST elevation and Q waves. They are also
seen in Prinzmetal angina.

Example 1:

Tall “tented” T waves present in the anteroseptal chest leads

Tall “hyperacute” T waves is seen in the anteroseptal chest leads

indicating ACS

Inverted T waves -Inverted T waves are seen in:

1. Normal finding in children
2. Persistent juvenile T wave pattern
3. Myocardial ischaemia and infarction (including Wellens
Syndrome)
4. Bundle branch block
5. Ventricular hypertrophy (‘strain’ patterns)
 Example 1:

Left ventricular hypertrophy (LVH) produces T-wave inversion in the

lateral leads I, aVL, V5-6 (left ventricular ‘strain’ pattern

Inferior T wave inversion (II, III, aVF) due to acute ischemia

Example 4:

Example 2:

Right ventricular hypertrophy produces T-wave inversion in the right

precordial leads V1-3 (right ventricular ‘strain’ pattern) and also the
inferior leads (II, III, aVF)

Biphasic T waves -Main causes of biphasic T waves are myocardial ischemia and
hypokalemia
Anterior T wave inversion with Q waves due to recent MI -The two waves go in opposite position

Example 3:

Biphasic T waves due to ischaemia: T waves go UP then DOWN

Biphasic T waves due to Hypokalemia: T waves go DOWN then UP

Flattened T waves -It is a non-specific finding and may represent ischemia or electrolyte Prolonged QT interval Causes of prolonged QT interval:
imbalance such as hypokalemia 1. Hypokalaemia
2. Hypomagnesaemia
QT interval 3. Hypocalcaemia
4. Hypothermia
Introduction -It is measured from the start of QRS complex to the end of T waves 5. Myocardial ischemia
-It represents ventricular depolarization and repolarization, 6. ROSC Post-cardiac arrest
effectively the period of ventricular systole from ventricular 7. Raised intracranial pressure
isovolumetric contraction to isovolumetric relaxation 8. Congenital long QT syndrome
-It is inversely proportional to the heart rate 9. Medications/Drugs

- Example 1:
-The QT interval shortens at faster heart rates and the QT interval
lengthens at slower heart rates
-Prolonged if QTc >440msec in men and >460msec in women
-QTc >500msec is associated with an increased risk of torsades de
pointes
-QTc is abnormally short if <350msec

Apparent QTc 500ms, prolonged QT interval due to hypokalemia

 Example 2:
Example 2:

Very short QTc (280ms) with tall, peaked T waves due to congenital
short QT syndrome. Congenital short QT syndrome (SQTS) is an
QTc 500ms due to congenital QT syndrome. High risk associated autosomal dominant inherited disorder of potassium channels
with torsades de pointes and sudden cardiac death. associated with an increased risk of paroxysmal atrial and ventricular
fibrillation and sudden cardiac death.
Management of torsades de pointes:
-If stable, give IV magnesium sulphate Short QT syndrome may be suggested by the presence of:
-If unstable, defibrillator -Lone atrial fibrillation in young adults
-Generally, stop all drugs that prolong QT interval and correct if -Family member with a short QT interval
there’s any electrolyte imbalance -Family history of sudden cardiac death
-ECG showing QTc < 350 ms with tall, peaked T waves
Short QT Causes of short QT interval: -Failure of the QT interval to increase as the heart rate slows
1. Hypercalcaemia
2. Congenital short QT syndrome
U waves
3. Digoxin effect
Introduction -It is related to afterdepolarization which follow repolarization
-The U wave is a small (0.5 mm) deflection immediately following
Example 1: the T wave
-It is usually in the same direction as the T wave.
-U wave is best seen in leads V2 and V3.

Normal features of U waves:

-The U wave normally goes in the same direction as the T wave
-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 65
bpm
-The voltage of the U wave is normally < 25% of the T-wave voltage:
Short QTc (260ms) due to hypercalcemia. Hypercalcaemia leads to disproportionally large U waves are abnormal
shortening of the ST segment and may be associated with the -Maximum normal amplitude of the U wave is 1-2 mm
appearance of Osborne waves

Example 2:

Abnormalities of U waves:
-Prominent U waves
-Inverted U waves Prominent U waves due to severe hypokalemia
Prominent U waves -Defined as >1-2mm or 25% of the height of the T wave Inverted U waves -U-wave inversion is abnormal (in leads with upright T waves)
-Causes included: -A negative U wave is highly specific for the presence of heart
1. Bradycardia disease
2. Severe hypokalemia -Common causes of inverted U waves:
3. Hypocalcemia 1. Coronary artery disease
4. Hypomagnesemia 2. Hypertension
5. Hypothermia 3. Valvular heart disease
6. Raised ICP 4. Congenital heart disease
7. Drugs such as digoxin, phenothiazines 5. Cardiomyopathy
8. Left ventricular hypertrophy 6. Hyperthyroidism
-In patients with presenting chest pain, inverted U waves are very
Example 1: specific sign of myocardial ischemia

Example 1:

Prominent U waves due to sinus bradycardia

 Inverted U waves in patient with unstable angina Abnormality -Elevation or depression of the J point is seen with the various causes
of ST segment abnormality.
-Elevation of the J point occurs with benign early repolarization
Example 2: -A positive deflection prior to the J point is termed a J wave (Osborn
wave) and is characteristically seen with hypothermia.

Delta waves
Introduction -The Delta wave is a slurred upstroke in the QRS complex often
Inverted U waves in patient with unstable angina associated with a short PR interval. It is most commonly associated
with pre-excitation syndrome such as WPW.
J point
Introduction -It is the junction between the termination of the QRS complex and
the beginning of the ST segment
-J point is present in all ECGs and marks the transition of QRS
complex to ST segment

Delta wave Example 1:

Wolf-Parkinson-White -It is defined as a congenital condition involving abnormal
syndrome conductive cardiac tissue between the atria and the ventricles that
provides a pathway for a reentrant tachycardia circuit, in association
with supraventricular tachycardia (SVT)
-Characteristics of WPW syndrome in ECG:
1. Short PR interval (< 120ms)
2. Broad QRS (> 100ms)
3. A slurred upstroke to the QRS complex (the delta wave)

ST depression in Lead II, III and aVF, inferior ischemia

Example 2:

Common ECG abnormalities

Myocardial ischemia -ECG ischemic changes:
1. Hyperacute T waves (early)
2. ST-segment elevation/ depression
3. Pathologic Q waves
4. T wave inversion
-It should present in 2 contiguous leads (side-by-side)
Widespread ST depression (leads I, II, V5-6) indicates
subendocardial ischaemia. Q wave in lead III with slightly elevated
 ST segment suggests the possibility of early inferior STEMI. hypotension and prescribing nitrates (GTN) can worsen the
condition
Posterior infarction -Look for reciprocal changes in anterior leads (V1-3):
1. ST depression in V1-3 Example 1:
2. Tall, broad R waves (>30ms)
3. Upright T waves
4. Dominant R wave (R/S ratio > 1) in V2
-These are the same ECG changes of a STEMI that have been
flipped:
1. ST elevation -> ST depression
2. Q waves -> dominant R waves
3. Inverted T waves -> upright T waves
-Flip the paper over and look through the back. This makes a
posterior STEMI look like a normal STEMI

Inferolateral STEMI. Posterior extension is suggested by:

-Horizontal ST depression in V1-3
-Tall, broad R waves (> 30ms) in V2-3
-Dominant R wave (R/S ratio > 1) in V2
-Upright T waves in V2-3

Example 2:

-Confirm by doing right-sided ECG at V7 (posterior axillary line),

V8 (tip of scapula), V9 (paraspinal line)

Marked ST elevation in V7-9 with Q-wave formation confirms

involvement of the posterior wall, making this an
inferior-lateral-posterior STEMI

Wellens syndrome -It is a pattern of deeply inverted or biphasic T waves in V2-3, which
is highly specific for a critical stenosis of the left anterior descending
artery (LAD)
-The rest of the ECG may be normal
-ECG normal at pain and ECG changes at pain-free period
-Pathophysiology: transient anterior ischemia
-Important to diagnose right ventricular infarct as it is susceptible to -Diagnostic criteria for Wellens syndrome:

1. Deeply-inverted or biphasic T waves in V2-3 (may extend to

V1-6)
2. Isoelectric or minimally-elevated ST segment (< 1mm)
3. No precordial Q waves
4. Preserved precordial R wave progression
5. Recent history of angina
6. ECG pattern present in pain-free state
7. Normal or slightly elevated serum cardiac markers
-Two patterns of T-wave abnormality in Wellens syndrome:
1. Type A: Biphasic, with initial positivity and terminal
Example 1:
negativity (25% of cases)

Biphasic precordial T waves with terminal negativity, most

prominent in V2-3. Wellens syndrome (Type A pattern)

2. Type B: Deeply and symmetrically inverted (75% of cases) Example 2:

There are deep, symmetrical T wave inversions throughout the

anterolateral leads (V1-6, I, aVL). Wellens syndrome (Type B
pattern)

AV nodal block -It is a conduction disease of AV node

-Three degrees of AV nodal block
-Wellen wave evolution: T wave changes can evolve from Type A to
B over time First degree AV block
-Every P wave is followed by a QRS
-PR interval >200msec (1 big square)
-PR interval is constant

-Causes of Mobitz 1:
1. Drugs: beta-blockers, calcium channel blockers, digoxin,
amiodarone
-Causes of first degree AV block: 2. Increased vagal tone (e.g. athletes)
1. Increased vagal tone 3. Inferior MI
2. Athletic training 4. Myocarditis
3. Inferior MI -It is usually a benign rhythm, causing minimal haemodynamic
4. AV nodal blocking drugs (beta-blockers, calcium channel disturbance and with low risk of progression to third degree heart
blockers, digoxin, amiodarone) block
-No specific treatment is needed if asymptomatic -Asymptomatic patients do not require treatment and symptomatic
patients usually respond to atropine
Example 1:
Example 1:

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

Example 2:

Progressive prolongation of PR interval, with a subsequent

non-conducted P wave

Mobitz 2 (Hay block)

PR interval > 300 ms, it is a sinus bradycardia with first degree AV -A form of 2nd degree AV block in which there is intermittent
block non-conducted P waves without progressive prolongation of the PR
interval
Second degree AV block
Mobitz 1 (Wenckebach Phenomenon)
-PR interval lengthens progressively followed by a dropped beat and
then the PR interval resets
-PR interval is longest immediately before dropped beat and the PR
interval is shortest immediately after dropped beat
-Causes of Mobitz 2:
1. Anterior MI (due to septal infarction with necrosis of the

bundle branches)
2. Idiopathic fibrosis of the conducting system (Lenègre-Lev
disease)
3. Cardiac surgery
-Mobitz II is much more likely than Mobitz I to be associated with
haemodynamic compromise, severe bradycardia and progression to
Every third P wave is almost entirely concealed within the T wave.
3rd degree heart block
(3:1 block)
-Mobitz II mandates immediate admission for cardiac monitoring,
backup temporary pacing and ultimately insertion of a permanent
Third degree block (complete heart block)
pacemaker
-Severe bradycardia due to absence of AV conduction
-The ECG demonstrates complete AV dissociation, with independent
Example 1:
atrial and ventricular rates

-There is AV dissociation, with the atrial rate (~100 bpm)

independent of the ventricular rate (~40 bpm)
-Complete heart block is essentially the end point of either Mobitz I
or Mobitz II AV block
-They require urgent admission for cardiac monitoring, backup
temporary pacing and usually insertion of a permanent pacemaker

Example 1:
Constant PR interval with intermittent non-conducted P waves
(Mobitz 2)

Fixed ratio AV blocks

-Second degree AV blocks with a fixed ratio of P waves : QRS
complex (eg. 2:1, 3:1)
-It can be a result of either Mobitz 1 or Mobitz 2 conduction

Example 1:

Non-conducted P waves are superimposed on the end of each T Atrial rate is ~60 bpm, ventricular rate is ~27 bpm, none of the atrial
wave (2:1 block) impulses appear to be conducted to the ventricles. It is a complete
heart block

Example 2: Bundle branch blocks -It leads to abnormal ventricular conduction -> wide QRS complex
-2 types of BBB: Right BBB and Left BBB
 Left bundle branch block (LBBB) -RSR’ pattern in V1-3 (“M-shaped” QRS complex)
Diagnostic criteria: -Wide, slurred S wave in lateral leads (I, aVL, V5-6)
-QRS duration > 120ms
-Dominant S wave in V1
-Broad “notched” (M-shaped) 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

-“WiLLiaM”
-Associated features may include: Left axis deviation (LAD), poor R
wave progression in precordial lead
-Causes of LBBB:
1. Aortic stenosis
2. Ischaemic heart disease
3. Hypertension
4. Dilated cardiomyopathy
5. Anterior MI
-“MoRRoW”
Example 1: -Associated features: Appropriate discordance with ST depression
and/or T-wave inversion in right precordial leads (V1-3)
-Causes of RBBB:
1. Right ventricular hypertrophy / cor pulmonale
2. Pulmonary embolism
3. Ischaemic heart disease
4. Rheumatic heart disease
5. Congenital heart disease

Example 1:

Broad notched R waves are best appreciated in leads aVL and I here.
There is absence of Q waves in leads V5-6.

Right bundle branch block (RBBB)

Diagnostic criteria:
-QRS duration > 120ms

Typical RSR’ pattern in V1-2, widened S waves in V4-6. RBBB

Tachycardia
Right axis deviation (+150 degrees), dominant R wave in V1 (> 7
Tachycardia 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
Narrow QRS Widened QRS T-wave inversion in V1-4. Typical features of RVH
Regular Irregular Regular Irregular Left ventricular hypertrophy
-Sinus -Atrial -Ventricular -Atrial Suspect LVH when:
tachycardia fibrillation tachycardia fibrillation -S wave depth in V1 plus tallest R wave in V5-6 >35mm (7 big
-Supraventricu -Atrial flutter -Supraventricu with squares)
lar tachycardia with variable lar tachycardia aberrancy/ -Left axis deviation
-Atrial flutter block with aberrancy WPW
2:1 -Multifocal -Polymorphic Voltage criteria in precordial leads:
-Junctional atrial ventricular -R wave in V4, V5 or V6 > 26 mm
tachycardia tachycardia tachycardia -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
Some discussed earlier at section Rhythm
Non-voltage criteria:
Right and Left Right ventricular hypertrophy -Increased R wave peak time > 50 ms in leads V5 or V6
ventricular hypertrophy Diagnostic criteria: -ST segment depression and T wave inversion in the left-sided leads:
-Right axis deviation of +110° or more. AKA the left ventricular ‘strain’ pattern
-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)

Example 1:

LVH by voltage criteria: S wave in V2 + R wave in V5 > 35 mm

Example 1:
 PR depression and ST elevation in V5

-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 Reciprocal PR elevation and ST depression in aVR
-These acute changes may be followed by:
Pericarditis -Inflammation of the pericardium secondary to infection, localised 1. T wave flattening
injury or systemic disorders producing characteristic chest pain, 2. T wave inversion
dyspnoea and serial ECG changes. 3. Normalisation of ECG
-Characteristics of ECG changes:
1. Widespread concave ST elevation and PR depression Example 1:
throughout most of the limb leads (I, II, III, aVL, aVF) and
precordial leads (V2-6)
2. Reciprocal ST depression and PR elevation in lead aVR (±
V1)
3. Sinus tachycardia is also common in acute pericarditis due to
pain and/or pericardial effusion

Widespread concave ST elevation and PR depression is present

throughout the precordial (V2-6) and limb leads (I, II, aVL, aVF).
There is reciprocal ST depression and PR elevation in aVR. The
diagnosis is acute pericarditis

Pulmonary embolism -Most common ECG findings: Sinus tachycardia (44%)

-Other findings:

1. Right axis deviation (16%)

2. RBBB (18%)
3. Right ventricular strain: T wave inversion and ST depression
in V1-4 (34%)
4. SI QIII TIII pattern: Deep S wave in lead I, Q wave in III,
inverted T wave in III (20%)
5. Atrial tachycardia (AF, atrial flutter, MAT etc in 8%)

Example 1:

Example 1:

Sinus tachycardia, RBBB, T-wave inversions in the right precordial

leads (V1-3) as well as lead III. Massive bilateral pulmonary
embolism

Hyperkalemia -Hyperkalemia is defined as a serum potassium level of > 5.2

mmol/L.
-ECG changes generally do not manifest until there is a moderate
degree of hyperkalaemia (≥ 6.0 mmol/L).
-The earliest manifestation of hyperkalemia is an increase in T wave
amplitude.
-The ECG changes are:
1. Peaked/tall-tented T waves Prolonged PR interval, tall-tented T waves, widened QRS complex.
2. P wave widening/flattening, PR prolongation Features of hyperkalemia
3. Bradyarrhythmias: sinus bradycardia, high-grade AV block
with slow junctional and ventricular escape rhythms, slow
AF
4. Conduction blocks (bundle branch block, fascicular blocks)
5. QRS widening with bizarre QRS morphology