ECG Rate

ECG Rhythm

ECG Axis

Lead positioning

P wave

Q Wave

R wave

T wave

U Wave

Osborn Wave (J Wave)

Delta Wave

Epsilon Wave

PR Interval

PR segment

QT Interval

ST Segment

J point

QRS complex

Left Atrial Enlargement

Right Atrial Enlargement

Bi-Atrial Enlargement


ECG Rate Interpretation

The usual paper speed is 25mm/sec:


 If a different paper speed is used, calculations will have to be modified appropriately.

Estimate the rate

There are multiple methods to estimate the rate:


Interpretation (adults)

Normal Heart Rates in Children


ECG Rhythm

The rhythm is best analysed by looking at a rhythm strip. On a 12 lead ECG this is usually a 10 second recording from Lead II. Confirm or corroborate any findings in this lead by checking the other leads. A longer rhythm strip, recorded perhaps recorded at a slower speed, may be helpful. A useful 7 step approach to ECG rhythm analysis is described.

1. Rate

  • Tachycardia or bradycardia?
  • Normal rate is 60-100/min.

2. Pattern of QRS complexes

  • Regular or irregular?
  • If irregular is it regularly irregular or irregularly irregular?

3. QRS morphology

  • Narrow complex — sinus, atrial or junctional origin.
  • Wide complex — ventricular origin, or supraventricular with aberrant conduction.

4. P waves

  • Absent — sinus arrest, atrial fibrillation
  • Present — morphology and PR interval may suggest sinus, atrial, junctional or even retrograde from the ventricles.

5. Relationship between P waves and QRS complexes

  • AV association (may be difficult to distinguish from  isorhythmic dissociation)
  • AV dissociation
    • complete — atrial and ventricular activity is always independent.
    • incomplete — intermittent capture.

6. Onset and termination

  • Abrupt — suggests re-entrant process.
  • Gradual — suggests increased automaticity.

7. Response to vagal manoeuvres

  • Sinus tachycardia, ectopic atrial tachydysrhythmia — gradual slowing during the vagal manoeuvre, but resumes on cessation.
  • AVNRT or AVRT — abrupt termination or no response.
  • Atrial fibrillation and atrial flutter — gradual slowing during the manoeuvre.
  • VT — no response.

Differential Diagnosis

Narrow Complex (Supraventricular) Tachycardias

Atrial Regular(Narrow Complex (Supraventricular) Tachycardias):-

  • Sinus tachycardia
  • Atrial tachycardia
  • Atrial flutter
  • Inappropriate sinus tachycardia
  • Sinus node re-entrant tachycardia

Atrial Irregular (Narrow Complex (Supraventricular) Tachycardias} :-

  • Atrial fibrillation
  • Atrial flutter with variable block
  • Multifocal atrial tachycardia


  • Atrioventricular re-entry tachycardia (AVRT)
  • AV nodal re-entry tachycardia (AVNRT)
  • Automatic junctional tachycardia

Broad Complex Tachycardias


  • Ventricular tachycardia
  • Antidromic atrioventricular re-entry tachycardia (AVRT).
  • Any regular supraventricular tachycardia with aberrant conduction — e.g. due to bundle branch block, rate-related aberrancy.

All regular BCTs should be considered to be VT until proven otherwise.


  • Ventricular fibrillation
  • Polymorphic VT
  • Torsades de Pointes
  • AF with Wolff-Parkinson-White syndrome
  • Any irregular supraventricular tachycardia with aberrant conduction — e.g. due to bundle branch block, rate-related aberrancy.


P waves present

Each P wave is followed by a QRS complex (= sinus node dysfunction)
  • Sinus bradycardia
  • Sinus node exit block
  • Sinus pause / arrest

Not every P wave is followed by a QRS complex (= AV node dysfunction)

  • AV block: 2nd degree, Mobitz I (Wenckebach)
  • AV block: 2nd degree, Mobitz II
  • AV block: 2nd degree, “fixed ratio blocks” (2:1, 3:1)
  • AV block: 2nd degree, “high grade AV block”
  • AV block: 3rd degree (complete heart block)

P waves absent

Narrow complexes

  • Junctional escape rhythm

Broad complexes

  • Ventricular escape rhythm

For escape rhythms to occur there must be a failure of sinus node impulse generation or transmission by the AV node. 


ECG Axis Interpretation

The diagram below illustrates the relationship between QRS axis and the frontal leads of the ECG.

  • Normal Axis = QRS axis between -30 and +90 degrees.
  • Left Axis Deviation = QRS axis less than -30 degrees.
  • Right Axis Deviation = QRS axis greater than +90 degrees.
  • Extreme Axis Deviation = QRS axis between -90 and 180 degrees (AKA “Northwest Axis”).

Methods of ECG Axis Interpretation

There are several complementary approaches to estimating QRS axis, which are summarised below:
  1. The Quadrant Method
  2. Leads I + II Analysis
  3. Combination of Quadrant and lead analysis
  4. The Isoelectric Lead

Method 1 – The Quadrant Method

The most efficient way to estimate axis is to look at leads I + aVF

Method 2 – Leads I + II

Another rapid method is to look at leads I + II.
  • A positive QRS in lead I puts the axis in roughly the same direction as lead I.



  • A positive QRS in lead II similarly aligns the axis with lead II.



  • Therefore, if leads I and II are both positive, the axis is between -30 and +90 degrees (i.e. normal axis).


Combining Methods 1 and 2

By combining these two methods, you can rapidly and accurately assess axis.


Method 3 – The Isoelectric Lead

This method allows a more precise estimation of QRS axis, using the axis diagram below.

Key Principles

  • If the QRS is positive in any given lead, the axis points in roughly the same direction as this lead.
  • If the QRS is negative in any given lead, the axis points in roughly the opposite direction to this lead.
  • If the QRS is isoelectric in any given lead (positive deflection = negative deflection), the axis is at 90 degrees to this lead.

Step 1. Find the isoelectric lead.

The isoelectric (equiphasic) lead is the frontal lead with zero net amplitude. This can be either:

  • A biphasic QRS where R wave height = Q or S wave depth.
  • A flat-line QRS with no discernible features.

Step 2. Find the positive leads. 

  • Look for the leads with the tallest R waves (or largest R/S ratios).

Step 3. Calculate the QRS axis. 

  • The QRS axis is at 90 degrees to the isoelectric lead, pointing in the direction of the positive leads.

This concept can be difficult to understand at first, and is best illustrated by some examples.

Case 1


Quadrant Method

  • Leads I + aVF are both positive.
  • This puts the axis in the left lower quadrant, between 0 and +90 degrees, i.e. normal axis.
  • Lead II is also positive, which confirms the normal axis.

 Isoelectric Lead Method

  • Lead aVL is isoelectric, being biphasic with similarly sized positive and negative deflections (no need to precisely measure this).
  • From the diagram above, we can see that aVL is located at -30 degrees.
  • The QRS axis must be ± 90 degrees from lead aVL, either at +60 or -120 degrees.
  • With leads I (0), II (+60) and aVF (+90) all being positive, we know that the axis must lie somewhere between 0 and +90 degrees.
  • This puts the QRS axis at +60 degrees.

Case 2


Quadrant Method

  • Lead I = negative.
  • Lead aVF = positive.
  • This puts the axis in the right lower quadrant, between +90 and +180 degrees, i.e. RAD.

Isoelectric Lead Method

  • Lead II (+60 degrees) is the isoelectric lead.
  • The QRS axis must be ± 90 degrees from lead II, at either +150 or -30 degrees.
  • The more rightward-facing leads III (+120) and aVF (+90) are positive, while aVL (-30) is negative.
  • This puts the QRS axis at +150 degrees.

This is an example of right axis deviation secondary to right ventricular hypertrophy.

Case 3


Quadrant Method

  • Lead I = positive.
  • Lead aVF = negative.
  • This puts the axis in the left upper quadrant, between 0 and -90 degrees, i.e. normal or LAD.
  • Lead II is neither positive nor negative (isoelectric), indicating borderline LAD.

Isoelectric Lead Method

  • Lead II (+60 degrees) is isoelectric.
  • The QRS axis must be ± 90 degrees from lead II, at either +150 or -30 degrees.
  • The more leftward-facing leads I (0) and aVL (-30) are positive, while lead III (+120) is negative.
  • This confirms that the axis is at -30 degrees.

This is an example of borderline left axis deviation due to inferior MI.

Case 4


Quadrant Method

  • Lead I = negative.
  • Lead aVF = negative.
  • This puts the axis in the upper right quadrant, between -90 and 180 degrees, i.e. extreme axis deviation.

NB. The presence of a positive QRS in aVR with negative QRS in multiple leads is another clue to the presence of extreme axis deviation. 

 Isoelectric Lead Method

  • The most isoelectric lead is aVL (-30 degrees).
  • The QRS axis must be at ± 90 degrees from aVL at either +60 or -120 degrees.
  • Lead aVR (-150) is positive, with lead II (+60) negative.
  • This puts the axis at -120 degrees.

This is an example of extreme axis deviation due to ventricular tachycardia.

Case 5


  • Lead I = isoelectric.
  • Lead aVF = positive.
  • This is the easiest axis you will ever have to calculate. It has to be at right angles to lead I and in the direction of aVF, which makes it exactly +90 degrees!

This is referred to as a “vertical axis”  and is seen in patients with emphysema who typically have a vertically orientated heart.


Vertical Heart in Emphysema 


Causes of Axis Deviation

Right Axis Deviation

  • Right ventricular hypertrophy
  • Acute right ventricular strain, e.g. due to pulmonary embolism
  • Lateral STEMI
  • Chronic lung disease, e.g. COPD
  • Hyperkalaemia
  • Sodium-channel blockade, e.g. TCA poisoning
  • Wolff-Parkinson-White syndrome
  • Dextrocardia
  • Ventricular ectopy
  • Secundum ASD – rSR’ pattern
  • Normal paediatric ECG
  • Left posterior fascicular block – diagnosis of exclusion
  • Vertically orientated heart – tall, thin patient

Left Axis Deviation

  • Left ventricular hypertrophy
  • Left bundle branch block
  • Inferior MI
  • Ventricular pacing /ectopy
  • Wolff-Parkinson-White Syndrome
  • Primum ASD – rSR’ pattern
  • Left anterior fascicular block – diagnosis of exclusion
  • Horizontally orientated heart – short, squat patient

Extreme Axis Deviation

  • Ventricular rhythms – e.g.VT, AIVR, ventricular ectopy
  • Hyperkalaemia
  • Severe right ventricular hypertrophy


Lead positioning

The ECG is one of the most useful investigations in medicine. Electrodes attached to the chest and/or limbs record small voltage changes as potential difference, which is transposed into a visual tracing

3-Electrode System

  • Uses 3 electrodes (RA, LA and LL)
  • Monitor displays the bipolar leads (I, II and III)
  • To get best results – Place electrodes on the chest wall equidistant from the heart (rather than the specific limbs)



5-Electrode System

  • Uses 5 electrodes (RA, RL, LA, LL and Chest)
  • Monitor displays the bipolar leads (I, II and III)
  • AND a single unipolar lead (depending on position of the brown chest lead (positions V1–6))


12-lead ECG

  • 10 electrodes required to produce 12-lead ECG
    • 4 Electrodes on all 4 limbs (RA, LL, LA, RL)
    • 6 Electrodes on precordium (V1–6)
  • Monitors 12 leads (V1–6), (I, II, III) and (aVR, aVF, aVL)
  • Allows interpretation of specific areas of the heart
    • Inferior (II, III, aVF)
    • Lateral (I, aVL, V5, V6)
    • Anterior (V1–4)



ECG electrode system



The P wave

  • The P wave is the first positive deflection on the ECG
  • It represents atrial depolarisation


Characteristics of the Normal Sinus P Wave


  • Smooth contour
  • Monophasic in lead II
  • Biphasic in V1


  • Normal P wave axis is between 0° and +75°
  • P waves should be upright in leads I and II, inverted in aVR


  • < 120 ms


  • < 2.5 mm in the limb leads,
  • < 1.5 mm in the precordial leads
Atrial abnormalities are most easily seen in the inferior leads (II, III and aVF) and lead V1, as the P waves are most prominent in these leads.

The Atrial Waveform – Relationship to the P wave

  • Atrial depolarisation proceeds sequentially from right to left, with the right atrium activated before the left atrium.
  • The right and left atrial waveforms summate to form the P wave.
  • The first 1/3 of the P wave corresponds to right atrial activation, the final 1/3 corresponds to left atrial activation; the middle 1/3 is a combination of the two.
  • In most leads (e.g. lead II), the right and left atrial waveforms move in the same direction, forming a monophasic P wave.
  • However, in lead V1 the right and left atrial waveforms move in opposite directions. This produces a biphasic P wave with the initial positive deflection corresponding to right atrial activation and the subsequent negative deflection denoting left atrial activation.
  • This separation of right and left atrial electrical forces in lead V1 means that abnormalities affecting each individual atrial waveform can be discerned in this lead. Elsewhere, the overall shape of the P wave is used to infer the atrial abnormality.

Normal P-wave Morphology – Lead II

  • The right atrial depolarisation wave (brown) precedes that of the left atrium (blue).
  • The combined depolarisation wave, the P wave, is less than 120 ms wide and less than 2.5 mm high.

Right Atrial Enlargement – Lead II

  • In right atrial enlargement, right atrial depolarisation lasts longer than normal and its waveform extends to the end of left atrial depolarisation.
  • Although the amplitude of the right atrial depolarisation current remains unchanged, its peak now falls on top of that of the left atrial depolarisation wave.
  • The combination of these two waveforms produces a P waves that is taller than normal (> 2.5 mm), although the width remains unchanged (< 120 ms).

 Left Atrial Enlargement – Lead II

  • In left atrial enlargement, left atrial depolarisation lasts longer than normal but its amplitude remains unchanged.
  • Therefore, the height of the resultant P wave remains within normal limits but its duration is longer than 120 ms.
  • A notch (broken line) near its peak may or may not be present (“P mitrale”).

Normal P-wave Morphology – Lead V1

The P wave is typically biphasic in V1, with similar sizes of the positive and negative deflections.


Right Atrial Enlargement – Lead V1

Right atrial enlargement causes increased height (> 1.5mm) in V1 of the initial positive deflection of the P wave.
NB. This patient also has evidence of right ventricular hypertrophy.

Left Atrial Enlargement – Lead V1

Left atrial enlargement causes widening (> 40ms wide) and deepening (> 1mm deep) in V1 of the terminal negative portion of the P wave.

Biatrial Enlargement

Biatrial enlargement is diagnosed when criteria for both right and left atrial enlargement are present on the same ECG.
The spectrum of P-wave changes in leads II and V1 with right, left and bi-atrial enlargement is summarised in the following diagram:

Common P Wave Abnormalities

Common P wave abnormalities include:

  • P mitrale (bifid P waves), seen with left atrial enlargement.
  • P pulmonale (peaked P waves), seen with right atrial enlargement.
  • P wave inversion, seen with ectopic atrial and junctional rhythms.
  • Variable P wave morphology, seen in multifocal atrial rhythms.

P mitrale

The presence of broad, notched (bifid) P waves in lead II is a sign of left atrial enlargement, classically due to mitral stenosis.


Bifid P waves (P mitrale) in left atrial enlargement

P Pulmonale

The presence of tall, peaked P waves in lead II is a sign of right atrial enlargement, usually due to pulmonary hypertension (e.g. cor pulmonale from chronic respiratory disease).

Peaked P waves (P pulmonale) due to right atrial enlargement


Inverted P Waves

P-wave inversion in the inferior leads indicates a non-sinus origin of the P waves.
When the PR interval is < 120 ms, the origin is in the AV junction (e.g. accelerated junctional rhythm):

Accelerated Junctional Rhythm  



When the PR interval is ≥ 120 ms, the origin is within the atria (e.g. ectopic atrial rhythm):

Ectopic Atrial Rhythm  




Variable P-Wave Morphology

The presence of multiple P wave morphologies indicates multiple ectopic pacemakers within the atria and/or AV junction.
If ≥ 3 different P wave morphologies are seen, then multifocal atrial rhythm is diagnosed:

If ≥ 3 different P wave morphologies are seen and the rate is ≥ 100, then multifocal atrial tachycardia (MAT) is diagnosed:

Multifocal Atrial Rhythm

If ≥ 3 different P wave morphologies are seen and the rate is ≥ 100, then multifocal atrial tachycardia (MAT) is diagnosed:

Multifocal Atrial Tachycardia


Q Wave

Normal Q wave:

  • A Q wave is any negative deflection that precedes an R wave



Normal Q wave in V6

Origin of the Q Wave

  • The Q wave represents the normal left-to-right depolarisation of the interventricular septum
  • Small ‘septal’ Q waves are typically seen in the left-sided leads (I, aVL, V5 and V6)

Q waves in different leads

  • Small Q waves are normal in most leads
  • Deeper Q waves (>2 mm) may be seen in leads III and aVR as a normal variant
  • Under normal circumstances, Q waves are not seen in the right-sided leads (V1-3)

Pathological Q Waves

Q waves are considered pathological if:

  • > 40 ms (1 mm) wide
  • > 2 mm deep
  • > 25% of depth of QRS complex
  • Seen in leads V1-3

Pathological Q waves usually indicate current or prior myocardial infarction.

Differential Diagnosis

  • Myocardial infarction
  • Cardiomyopathies — Hypertrophic (HOCM), infiltrative myocardial disease
  • Rotation of the heart — Extreme clockwise or counter-clockwise rotation
  • Lead placement errors — e.g. upper limb leads placed on lower limbs


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





Inferior Q waves (II, III, aVF) with T-wave inversion due to previous MI  







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






Anterior Q waves (V1-4) with ST elevation due to acute MI 







Anterior Q waves (V1-4) with T-wave inversion due to recent MI




Loss of normal Q waves

  • The absence of small septal Q waves in leads V5-6 should be considered abnormal.
  • Absent Q waves in V5-6 is most commonly due to LBBB.


Abnormalities of the R wave

Abnormalities of the R wave:

 Three R wave abnormalities

  1. Dominant R wave in V1
  2. Dominant R wave in aVR
  3. Poor R wave progression

Dominant R wave in V1

Causes of Dominant R wave in V1

  • Normal in children and young adults
  • Right Ventricular Hypertrophy (RVH)
    • Pulmonary Embolus
    • Persistence of infantile pattern
    • Left to right shunt
  • Right Bundle Branch Block (RBBB)
  • Posterior Myocardial Infarction (ST elevation in Leads V7, V8, V9)
  • Wolff-Parkinson-White (WPW) Type A
  • Incorrect lead placement (e.g. V1 and V3 reversed)
  • Dextrocardia
  • Hypertrophic cardiomyopathy
  • Dystrophy
    • Myotonic dystrophy
    • Duchenne Muscular dystrophy

Examples of Dominant R wave in V1

Normal paediatric ECG (2 yr old)



Right Ventricular Hypertrophy (RVH)



Right Bundle Branch Block



Right Bundle Branch Block MoRRoW 


Posterior MI

WPW (type A)


Leads V1 and V3 reversed 


Leads V1 and V3 reversed

Muscular dystrophy



Dominant R wave in aVR

  1. Poisoning with sodium-channel blocking drugs (e.g. TCAs)
  2. Dextrocardia
  3. Incorrect lead placement (left/right arm leads reversed)
  4. Commonly elevated in ventricular tachycardia (VT)

Examples of Dominant R wave in aVR<

Poisoning with sodium-channel blocking drugs


Na Channel blockade with dominant aVR R wave




This ECG shows all the classic features of dextrocardia:

Left arm/right arm lead reversal



Lead reversal reversed




The most common cause of a dominant R wave in aVR is incorrect limb lead placement, with reversal of the left and right arm electrodes. This produces a similar pattern to dextrocardia in the limb leads but with normal R-wave progression in the chest leads.
With LA/RA lead reversal:

Ventricular Tachycardia



Poor R wave progression

Poor R wave progression is described with an R wave ≤ 3 mm inV3 and is caused by:
  • Prior anteroseptal MI
  • LVH
  • Inaccurate lead placement
  • May be a normal variant


Poor R wave progression 

Note that absent R wave progression is characteristically seen in dextrocardia (see previous ECG). 


T wave

  • The T wave is the positive deflection after each QRS complex.
  • It represents ventricular repolarisation.

Characteristics of the normal T wave

  • Upright in all leads except aVR and V1
  • Amplitude < 5mm in limb leads, < 15mm in precordial leads
  • Duration (see QT interval)

T wave abnormalities

  • Hyperacute T waves
  • Inverted T waves
  • Biphasic T waves
  • ‘Camel Hump’ T waves
  • Flattened T waves

Peaked T waves

Tall, narrow, symmetrically peaked T-waves are characteristically seen in hyperkalaemia

Peaked T waves due to hyperkalaemia

Hyperacute T waves

Broad, asymmetrically peaked or ‘hyperacute’ T-waves 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 with Prinzmetal angina.

Hyperacute T waves due to anterior STEMI

Loss of precordial T-wave balance

Loss of precordial T-wave balance occurs when the upright T wave is larger than that in V6. This is a type of hyperacute T wave.

Inverted T waves

Inverted T waves are seen in the following conditions:

  • Normal finding in children
  • Persistent juvenile T wave pattern
  • Myocardial ischaemia and infarction
  • Bundle branch block
  • Ventricular hypertrophy (‘strain’ patterns)
  • Pulmonary embolism
  • Hypertrophic cardiomyopathy
  • Raised intracranial pressure

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).

Paediatric T waves

Inverted T-waves in the right precordial leads (V1-3) are a normal finding in children, representing the dominance of right ventricular forces

Normal pattern of T-wave inversions in a 2-year old boy


Persistent Juvenile T-wave Pattern

T-wave inversions in the right precordial leads may persist into adulthood and are most commonly seen in young Afro-Caribbean women. Persistent juvenile T-waves are asymmetric, shallow (<3mm) and usually limited to leads V1-3.

Persistent juvenile T-waves in an adult


Myocardial Ischaemia and Infarction

T-wave inversions due to myocardial ischaemia or infarction occur in contiguous leads based on the anatomical location of the area of ischaemia/infarction:


Inferior T wave inversion due to acute ischaemia


Inferior T wave inversion with Q waves due to prior inferior MI


T wave inversion in the lateral leads due to acute ischaemia


Anterior T wave inversion with Q waves due to recent anterior MI


Bundle Branch Block

Left Bundle Branch Block

Left bundle branch block produces T-wave inversion in the lateral leads I, aVL and V5-6.

Lateral T wave inversion due to LBBB


Right Bundle Branch Block

Right bundle branch block produces T-wave inversion in the right precordial leads V1-3. 


T-wave inversion in the right precordial leads due to RBBB


Ventricular Hypertrophy

Left Ventricular Hypertrophy

Left ventricular hypertrophy produces T-wave inversion in the lateral leads I, aVL, V5-6 (left ventricular ‘strain’ pattern), with a similar morphology to that seen in LBBB. 


Lateral T wave inversion due to LVH


Right Ventricular Hypertrophy

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) 


T wave inversion in the inferior and right precordial leads due to RVH


Pulmonary Embolism

Acute right heart strain (e.g. secondary to massive pulmonary embolism) produces a similar pattern to RVH, with T-wave inversions in the right precordial (V1-3) and inferior (II, III, aVF) leads


T wave inversion in the inferior and right precordial leads in a patient with bilateral PEs



Deep T wave inversion in V1-3 with RBBB in a patient with massive PE 


Pulmonary embolism may also produce T-wave inversion in lead III as part of the SI QIII TIII pattern (S wave in lead I, Q wave in lead III, T-wave inversion in lead III).


SI QIII TIII pattern in acute PE


Hypertrophic Cardiomyopathy (HOCM)

HOCM is associated with deep T wave inversions in all the precordial leads.


T wave inversion in V1-6 due to HOCM


Raised intracranial pressure

Events causing a sudden rise in ICP (e.g. subarachnoid haemorrhage) produce widespread deep T-wave inversions with a bizarre morphology.


Widespread deep T wave inversion due to SAH


Biphasic T waves

There are two main causes of biphasic T waves:

  • Myocardial ischaemia
  • Hypokalaemia

The two waves go in opposite directions:

  • Ischaemic T waves go up then down
  • Hypokalaemic T waves go down then up

Ischaemia – up then down


Biphasic T waves due to ischaemia


Hypokalaemia – down then up

Biphasic T waves due to hypokalaemia


Wellens’ Syndrome

Wellens’ syndrome is a pattern of inverted or biphasic T waves in V2-3 (in patients presenting with ischaemic chest pain) that is highly specific for critical stenosis of the left anterior descending artery.

There are two patterns of T-wave abnormality in Wellens’ syndrome:

  • Type 1 Wellens’ T-waves are deeply and symmetrically inverted
  • Type 2 Wellens’ T-waves are biphasic, with the initial deflection positive and the terminal deflection negative

Wellens’ Type 1




Wellens’ Type 2



‘Camel hump’ T waves

This is a term used by the great ECG lecturer and Emergency Physician Amal Mattu to describe T-waves that have a double peak or ‘camel hump’ appearance.

There are two causes for camel hump T waves:

  • Prominent U waves fused to the end of the T wave, as seen in severe hypokalaemia
  • Hidden P waves embedded in the T wave, as seen in sinus tachycardia and various types of heart block

Prominent U waves due to severe hypokalaemia 




Hidden P waves in sinus tachycardia 


Hidden P waves in marked 1st degree heart block 




Hidden P waves in 2nd degree heart block with 2:1 conduction 




Flattened T waves

Flattened T waves are a non-specific finding, but may represent

  • ischaemia (if dynamic or in contiguous leads) or
  • electrolyte abnormality, e.g. hypokalaemia (if generalised).


Dynamic T-wave flattening due to anterior ischaemia (above). T waves return to normal once the ischaemia resolves (below).

Dynamic T wave flattening due to anterior ischaemia 




T waves return to normal as ischaemia resolves 





Note generalised T-wave flattening with prominent U waves in the anterior leads (V2 and V3).


T wave flattening due to hypokalaemia 


U Wave

The U wave is a small (0.5 mm) deflection immediately following the T wave, usually in the same direction as the T wave. It is best seen in leads V2 and V3.

Normal U Wave

Features of Normal 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: disproportionally large U waves are abnormal
  • Maximum normal amplitude of the U wave is 1-2 mm

Abnormalities of the U wave

  • Prominent U waves
  • Inverted U waves

Prominent U waves

  • U waves are prominent if > 1-2mm or 25% of the height of the T wave.
  • The most common cause of prominent U waves is bradycardia.
  • Abnormally prominent U waves are characteristically seen in severe hypokalaemia.

Prominent U waves may also be seen with:

  • Hypocalcaemia
  • Hypomagnesaemia
  • Hypothermia
  • Raised intracranial pressure
  • Left ventricular hypertrophy
  • Hypertrophic cardiomyopathy

The following drugs may cause prominent U waves:

  • Digoxin
  • Phenothiazines (thioridazine)
  • Class Ia antiarrhythmics (quinidine, procainamide)
  • Class III antiarrhythmics (sotalol, amiodarone)

Note that many of the conditions causing prominent U waves will also cause a long QT.

Prominent U waves due to sinus bradycardia

Prominent U waves in a patient with marked sinus bradycardia due to anorexia nervosa



Prominent U waves due to hypokalaemia

Prominent U waves in a patient with a K+ of 1.9





Prominent U waves due to digoxin

Prominent U waves in a patient taking digoxin





Prominent U waves due to quinidine

Prominent U waves in a patient receiving quinidine




Inverted U waves

  • U-wave inversion is abnormal (in leads with upright T waves)
  • A negative U wave is highly specific for the presence of heart disease

The main causes of inverted U waves are:

  • Coronary artery disease
  • Hypertension
  • Valvular heart disease
  • Congenital heart disease
  • Cardiomyopathy
  • Hyperthyroidism

In patients presenting with chest pain, inverted U waves:

  • Are a very specific sign of myocardial ischaemia
  • May be the earliest marker of unstable angina and evolving myocardial infarction
  • Have been shown to predict a ≥ 75% stenosis of the LAD / LMCA and the presence of left ventricular dysfunction

Inverted U waves due to unstable angina

Inverted U waves in a patient with unstable angina.  





Inverted U waves due to Prinzmetal’s angina

Inverted U waves in a patient with Prinzmetal’s angina.  




Inverted U waves due to NSTEMI

Note the subtle U-wave inversion in the lateral leads (I, V5 and V6) in this patient with a NSTEMI; these were the only abnormal findings on his ECG.

Inverted U waves in a patient with a NSTEMI  




Osborn Wave (J Wave)



  • Characteristically seen in hypothermia (typically T<30C), but they are not pathognomonic.
  • J waves may be seen in a number of other conditions:
    • Normal variant
    • Hypercalcaemia
    • Medications
    • Neurological insults such as intracranial hypertension, severe head injury and subarachnoid haemorrhage
    • Le syndrome d’Haïssaguerre (idiopathic VF)



The height of the J wave is roughly proportional to the degree of hypothermia:

Subtle J waves in mild hypothermia (temp 32.5°C)

J waves in mild hypothermia 




J waves in moderate hypothermia (temp 30°C)

J waves in moderate hypothermia 





Marked J waves in severe hypothermia (temp < 27°C)

J waves in severe hypothermia 



Delta Wave

The characteristic ECG findings in the Wolff-Parkinson-White syndrome are:

Delta wave





Negative delta waves (e.g. seen in lead aVR) 




Epsilon Wave


Examples of Epsilon Waves






Arrhythmogenic Right Ventricular Dysplasia

The ECG changes in ARVD include:

  • Epsilon wave (most specific finding, seen in 30% of patients)
  • T wave inversions in V1-3 (85% of patients)
  • Prolonged S-wave upstroke of 55ms in V1-3 (95% of patients)
  • Localised QRS widening of 110ms in V1-3
  • Paroxysmal episodes of ventricular tachycardia with a LBBB morphology

ECG Cases


The following 12-lead ECG is a typical example of ARVD.

Prolonged S-wave upstroke in ARVD

Case 2
VT with LBBB morphology due to ARVD


PR Interval

  • The PR interval is the time from the onset of the P wave to the start of the QRS complex.
  • It reflects conduction through the AV node.

PR interval

Prolonged PR Interval – AV block (PR >200ms)

  • Delayed conduction through the AV node
  • May occur in isolation or co-exist with other blocks (e.g., second-degree AV block, trifascicular block)


First degree AV block

Sinus rhythm with marked 1st degree heart block (PR interval 340ms) 




Second degree AV block (Mobitz I) with prolonged PR interval 


Second degree heart block, Mobitz type I (Wenckeback phenomenon). Note how the baseline PR interval is prolonged, and then further prolongs with each successive beat, until a QRS complex is dropped. The PR interval before the dropped beat is the longest (340ms), while the PR interval after the dropped beat is the shortest (280ms).



Short PR interval (<120ms)

A short PR interval is seen with:

  • Preexcitation syndromes.
  • AV nodal (junctional) rhythm.

Pre-excitation syndromes

  • Wolff-Parkinson-White (WPW) and Lown-Ganong-Levine (LGL) syndromes.
  • These involve the presence of an accessory pathway connecting the atria and ventricles.
  • The accessory pathway conducts impulses faster than normal, producing a short PR interval.
  • The accessory pathway also acts as an anatomical re-entry circuit, making patients susceptible to re-entry tachyarrhythmias.
  • Patients present with episodes of paroxsymal supraventricular tachycardia (SVT), specifically atrioventricular re-entry tachycardia (AVRT), and characteristic features on the resting 12-lead ECG.

Wolff-Parkinson-White syndrome

The characteristic features of Wolff-Parkinson-White syndrome are a short PR interval, broad QRS and a slurred upstroke to the QRS complex, the delta wave.

Short PR (<120ms), broad QRS and delta waves in WPW syndrome

Lown-Ganong-Levine syndrome

The features of LGL syndrome are a very short PR interval with normal P waves and QRS complexes and absent delta waves.

Short PR interval with normal QRS complexes in LGL syndrome

AV nodal (junctional) rhythm

  • Junctional rhythms are narrow complex, regular rhythms arising from the AV node.
  • P waves are either absent or abnormal (e.g. inverted) with a short PR interval (=retrograde P waves)

Accelerated junctional rhythm demonstrating inverted P waves with a short PR interval (retrograde P waves)  



PR segment

The PR segment is the flat, usually isoelectric segment between the end of the P wave and the start of the QRS complex.

PR segment abnormalities occur in two main conditions:

  • Pericarditis
  • Atrial ischaemia


The characteristic changes of acute pericarditis are:

  • PR segment depression.
  • Widespread concave (‘saddle-shaped’) ST elevation.
  • Reciprocal ST depression and PR elevation in aVR and V1
  • Absence of reciprocal ST depression elsewhere.

NB. PR segment changes are relative to the baseline formed by the T-P segment.

Typical ECG of acute pericarditis.

PR segment depression in V5 due to acute pericarditis (note there is also some concave ST elevation)

PR elevation in aVR due to acute pericarditis (note the reciprocal ST depression)


EMQ wersja dla Opiekuna

Jak punktować odpowiedzi:

Atrial ischaemia

  • PR segment elevation or depression in patients with myocardial infarction indicates concomitant atrial ischaemia or infarction.
  • This finding has been associated with poor outcomes following MI, increased risk for the development of atrioventricular block, supraventricular arrhythmias and cardiac free-wall rupture.

Liu’s criteria for diagnosing atrial ischaemia / infarction include:

  • PR elevation >0.5 mm in V5 & V6 with reciprocal PR depression in V1 & V2
  • PR elevation >0.5 mm in lead I with reciprocal PR depression in leads II & III
  • PR depression >1.5 mm in the precordial leads
  • PR depression >1.2 mm in leads I, II, & III
  • Abnormal P wave morphology: M-shaped,W-shaped,irregular,or notched (minor criteria)
PR depression in inferior STEMI indicating concomitant atrial infarction

Profound PR-segment depression in inferior leads with (A) and without (B) clear-cut TP segment in acute inferior myocardial infarction. Note also ST-segment elevation in inferior leads.

Measurement of PR depression

Measurement of PR-segment depression with (A) and with- out (B) clear-cut TP segment.


QT Interval

The QT interval is inversely proportional to heart rate:

  • The QT shortens at faster heart rates
  • The QT lengthens at slower heart rates
  • An abnormally prolonged QT is associated with an increased risk of ventricular arrhythmias, especially Torsades de Pointes.
  • The recently described congenital short QT syndrome has been found to be associated with an increased risk of paroxysmal atrial and ventricular fibrillation and sudden cardiac death.

How to measure QT

  • The QT interval should be measured in either lead II or V5-6
  • Several successive beats should be measured, with the maximum interval taken
  • Large U waves (> 1mm) that are fused to the T wave should be included in the measurement
  • Smaller U waves and those that are separate from the T wave should be excluded
  • The maximum slope intercept method is used to define the end of the T wave (see below)

The QT interval is defined from the beginning of the QRS complex to the end of the T wave. The maximum slope intercept method defines the end of the T wave as the intercept between the isoelectric line with the tangent drawn through the maximum down slope of the T wave (left). When notched T waves are present (right), the QT interval is measured from the beginning of the QRS complex extending to the intersection point between the isoelectric line and the tangent drawn from the maximum down slope of the second notch, T2

Corrected QT

  • The corrected QT interval (QTc) estimates the QT interval at a heart rate of 60 bpm.
  • This allows comparison of QT values over time at different heart rates and improves detection of patients at increased risk of arrhythmias.

There are multiple formulas used to estimate QTc (see below). It is not clear which formula is the most useful.

  • Bazett’s formula: QTC = QT / √ RR
  • Fredericia’s formula: QTC = QT / RR 1/3
  • Framingham formula: QTC = QT + 0.154 (1 – RR)
  • Hodges formula: QTC = QT + 1.75 (heart rate – 60)

NB. The RR interval is given in seconds (RR interval = 60 / heart rate).

  • Bazett’s formula is the most commonly used due to its simplicity. It over-corrects at heart rates > 100 bpm and under-corrects at heart rates < 60 bpm, but provides an adequate correction for heart rates ranging from 60 – 100 bpm.
  • At heart rates outside of the 60 – 100 bpm range, the Fredericia or Framingham corrections are more accurate and should be used instead.
  • If an ECG is fortuitously captured while the patient’s heart rate is 60 bpm, the absolute QT interval should be used instead!

There are now multiple i-phone apps that will calculate QTc for you (e.g. MedCalc), and the website has a quick and easy QTc calculator that is free to use.

Normal QTc values

  • QTc is prolonged if > 440ms in men or > 460ms in women
  • QTc > 500 is associated with increased risk of torsades de pointes
  • QTc is abnormally short if < 350ms
  • A useful rule of thumb is that a normal QT is less than half the preceding RR interval

Causes of a prolonged QTc (>440ms)

  • Hypokalaemia
  • Hypomagnesaemia
  • Hypocalcaemia
  • Hypothermia
  • Myocardial ischemia
  • Post-cardiac arrest
  • Raised intracranial pressure
  • Congenital long QT syndrome


Apparent QTc 500ms – prominent U waves in precordial leads (hypokalaemia (K+ 1.9))




QTc 510 ms secondary to hypomagnesaemia 




QTc 510ms due to hypocalcaemia 



QTc 620 ms due to severe hypothermia

Myocardial Ischaemia


QTc 495 ms due to hyperacute MI

Raised ICP

QTc 630ms with widespread T wave inversion due to subarachnoid haemorrhage

Congenital Long QT Syndrome

QTc 550ms due to congenital long QT syndrome

Causes of a short QTc (<350ms)

  • Hypercalcaemia
  • Congenital short QT syndrome
  • Digoxin effect


Hypercalcaemia leads to shortening of the ST segment and may be associated with the appearance of Osborne waves.

Marked shortening of the QTc (260ms) due to hypercalcaemia


Congenital short QT syndrome

Very short QTc (280ms) with tall, peaked T waves due to congenital short QT syndrome

Short QT syndrome may be suggested by the presence of:

Very short QT (< 300ms) with peaked T waves in two patients with SQTS



Short QT interval due to digoxin (QT 260 ms, QTc 320ms approx)

QT interval scale

Viskin (2009) proposes the use of a ‘QT interval scale’ to aid diagnosis of patients with short and long QT syndromes (once reversible causes have been excluded):

QT interval scale

Drug-induced QT-Prolongation and Torsades

  • In the context of acute poisoning with QT-prolonging agents, the risk of TdP is better described by the absolute rather than corrected QT.
  • More precisely, the risk of TdP is determined by considering both the absolute QT interval and the simultaneous heart rate (i.e. on the same ECG tracing).
  • These values are then plotted on the QT nomogram (below) to determine whether the patient is at risk of TdP.
  • A QT interval-heart rate pair that plots above the line indicates that the patient is at risk of TdP.
  • From the nomogram, you can see that QTc-prolonging drugs that are associated with a relative tachycardia (e.g. quetiapine) are much less likely to cause TdP than those that are associated with a relative bradycardia (e.g. amisulpride).


The ST Segment

Causes of ST Segment Elevation


Morphology of the Elevated ST segment

Myocardial Infarction

Acute STEMI may produce ST elevation with either concave, convex or obliquely straight morphology




ST Segment Morphology in Other Conditions










LV aneurysm








Patterns of ST Elevation

Acute ST elevation myocardial infarction (STEMI)

Causes ST segment elevation and Q-wave formation in contiguous leads, either:
  • Septal (V1-2)
  • Anterior (V3-4)
  • Lateral (I + aVL, V5-6)
  • Inferior (II, III, aVF)
  • Right ventricular (V1, V4R)
  • Posterior (V7-9)

There is usually reciprocal ST depression in the electrically opposite leads. For example, STE in the high lateral leads I + aVL typically produces reciprocal ST depression in lead III (see example below).


Anterolateral STEMI 


Coronary Vasospasm (Prinzmetal’s angina)

  • This causes a pattern of ST elevation that is very similar to acute STEMI — i.e. localised ST elevation with reciprocal ST depression occurring during episodes of chest pain.
  • However, unlike acute STEMI the ECG changes are transient, reversible with vasodilators and not usually associated with myocardial necrosis.
  • It may be impossible to differentiate these two conditions based on the ECG alone.




Pericarditis causes widespread concave (“saddleback”) ST segment elevation with PR segment depression in multiple leads, typically involving I, II, III, aVF, aVL, and V2-6. There is reciprocal ST depression and PR elevation in leads aVR and V1. Spodick’s sign — a downward sloping TP segment — may also be seen.

Benign Early Repolarization


Benign Early Repolarization

BER causes mild ST elevation with tall T-waves mainly in the precordial leads. Is a normal variant commonly seen in young, healthy patients. There is often notching of the J-point — the “fish-hook” pattern. The ST changes may be more prominent at slower heart rates and disappear in the presence of tachycardia.

Left Bundle Branch Block


Left Bundle Branch Block

In left bundle branch block, the ST segments and T waves show “appropriate discordance” — i.e. they are directed opposite to the main vector of the QRS complex. This produces ST elevation and upright T waves in leads with a negative QRS complex (dominant S wave), while producing ST depression and T wave inversion in leads with a positive QRS complex (dominant R wave).

Left Ventricular Hypertrophy


LVH causes a similar pattern of repolarization abnormalities as LBBB, with ST elevation in the leads with deep S-waves (usually V1-3) and ST depression/T-wave inversion in the leads with tall R waves (I, aVL, V5-6).

Ventricular Aneurysm


Ventricular Aneurysm

This is an ECG pattern of residual ST elevation and deep Q waves seen in patients with previous myocardial infarction. It is associated with extensive myocardial damage and paradoxical movement of the left ventricular wall during systole.

Brugada Syndrome


Brugada syndrome
This in an inherited channelopathy (a disease of myocardial sodium channels) that leads to paroxysmal ventricular arrhythmias and sudden cardiac death in young patients. The tell-tale sign on the resting ECG is the “Brugada sign” — ST elevation and partial RBBB in V1-2 with a “coved” morphology.
  • There is ST elevation and partial RBBB in V1-2 with a coved morphology — the “Brugada sign”.


Ventricular Paced Rhythm


AV Sequential Pacing

Ventricular pacing (with a pacing wire in the right ventricle) causes ST segment abnormalities identical to that seen in LBBB. There is appropriate discordance, with the ST segment and T wave directed opposite to the main vector of the QRS complex.


Raised Intracranial Pressure


ST elevation due to traumatic brain injury 

Raised ICP (e.g. due to intracranial haemorrhage, traumatic brain injury) may cause ST elevation or depression that simulates myocardial ischaemia or pericarditis. More commonly, raised ICP is associated with widespread, deep T-wave inversions (“cerebral T waves”).

  • Widespread ST elevation with concave (pericarditis-like) morphology in a patient with severe traumatic brain injury.

Less Common Causes of ST segment Elevation

  • Pulmonary embolism and acute cor pulmonale (usually in lead III)
  • Acute aortic dissection (classically causes inferior STEMI due to RCA dissection)
  • Hyperkalaemia
  • Sodium-channel blocking drugs (secondary to QRS widening)
  • J-waves (hypothermia, hypercalcaemia)
  • Following electrical cardioversion
  • Others: Cardiac tumour, myocarditis, pancreas or gallbladder disease

Transient ST elevation after DC cardioversion from VF 





J waves in hypothermia simulating ST elevation 




Causes of ST Depression

  • Myocardial ischaemia / NSTEMI
  • Reciprocal change in STEMI
  • Posterior MI
  • Digoxin effect
  • Hypokalaemia
  • Supraventricular tachycardia
  • Right bundle branch block
  • Right ventricular hypertrophy
  • Left bundle branch block
  • Left ventricular hypertrophy
  • Ventricular paced rhythm

 Morphology of ST Depression

  • ST depression can be either upsloping, downsloping, or horizontal.
  • Horizontal or downsloping ST depression ≥ 0.5 mm at the J-point in ≥ 2 contiguous leads indicates myocardial ischaemia (according to the 2007 Task Force Criteria).
  • Upsloping ST depression in the precordial leads with prominent “De Winter’s” T waves is highly specific for occlusion of the LAD.
  • Reciprocal change has a morphology that resembles “upside down” ST elevation and is seen in leads electrically opposite to the site of infarction.
  • Posterior MI manifests as horizontal ST depression in V1-3 and is associated with upright T waves and tall R waves.


ST depression: upsloping (A), downsloping (B), horizontal (C)


ST segment morphology in myocardial ischaemia








Reciprocal change


ST elevation in III

Reciprocal change in aVL

ST segment morphology in posterior MI

Patterns of ST depression

Myocardial Ischaemia

ST depression due to subendocardial ischaemia may be present in a variable number of leads and with variable morphology. It is often most prominent in the left precordial leads V4-6 plus leads I, II and aVL. Widespread ST depression with ST elevation in aVR is seen in left main coronary artery occlusion and severe triple vessel disease.


LMCA Occlusion  

NB. ST depression localised to the inferior or high lateral leads is more likely to represent reciprocal change than subendocardial ischaemia. The corresponding ST elevation may be subtle and difficult to see, but should be sought. 


Reciprocal Change

ST elevation during acute STEMI is associated with simultaneous ST depression in the electrically opposite leads:

  • Inferior STEMI produces reciprocal ST depression in aVL (± lead I).
  • Lateral or anterolateral STEMI produces reciprocal ST depression in III and aVF (± lead II).
  • Reciprocal ST depression in V1-3 occurs with posterior infarction (see below)

Reciprocal ST depression in aVL with inferior STEMI 














Reciprocal ST depression in III and aVF with high lateral STEMI  




Posterior Myocardial Infarction

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.

Posterior MI  



De Winters T Waves

This pattern of up-sloping ST depression with symmetrically peaked T waves in the precordial leads is considered to be a STEMI equivalent, and is highly specific for an acute occlusion of the LAD.

De Winter’s T Waves 




Digoxin Effect

Treatment with digoxin causes downsloping ST depression with a “sagging”  morphology, reminiscent of Salvador Dali’s moustache.



Hypokalaemia causes widespread downsloping ST depression with T-wave flattening/inversion, prominent U waves and a prolonged QU interval






Right ventricular hypertrophy

RVH causes ST depression and T-wave inversion in the right precordial leads V1-3.

Right ventricular hypertrophy 




Right Bundle Branch Block

RBBB may produce a similar pattern of repolarisation abnormalities to RVH, with ST depression and T wave inversion in V1-3.

Right bundle branch block 




Supraventricular tachycardia

Supraventricular tachycardia (e.g. AVNRT) typically causes widespread horizontal ST depression, most prominent in the left precordial leads (V4-6). This rate-related ST depression does not necessarily indicate the presence of myocardial ischaemia, provided that it resolves with treatment.


AV-nodal re-entry tachycardia


J point


  • Elevation or depression of the J point is seen with the various causes of ST segment abnormality.
  • Notching of the J point occurs with benign early repolarisation.
  • A positive deflection at the J point is termed a J wave (Osborn wave) and is characteristically seen with hypothermia.


QRS Complex Morphology

Main Features to Consider

  1. Width of the complexes: Narrow versus broad.
  2. Voltage (height) of the complexes.
  3. Spot diagnoses: Specific morphology patterns that are important to recognise.

QRS Width

  • 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 may be due to aberrant conduction of supraventricular complexes (e.g. due to bundle branch block, hyperkalaemia or sodium-channel blockade).

Example ECG showing both narrow and broad complexes:

Sinus rhythm with frequent ventricular ectopic beats (VEBs) in a pattern of ventricular bigeminy. The narrow beats are sinus in origin, the broad complexes are ventricular. 





Narrow Complexes

Narrow (supraventricular) complexes arise from three main places:

  • Sino-atrial node (= normal P wave)
  • Atria (= abnormal P wave / flutter wave / fibrillatory wave)
  • AV node / junction (= either no P wave or an abnormal P wave with a PR interval < 120 ms)

Examples of Narrow Complex Rhythms:

Sinus rhythm: Each narrow complex is preceded by a normal P wave.


Atrial flutter: Narrow QRS complexes are associated with regular flutter waves. 




Junctional tachycardia: Narrow QRS complexes with no visible P waves. 





Broad Complexes

  • A QRS duration > 100 ms is abnormal
  • A QRS duration > 120 ms is required for the diagnosis of bundle branch block or ventricular rhythm

Broad complexes may be ventricular in origin or due to aberrant conduction secondary to:

  • Bundle branch block
  • Hyperkalaemia
  • Poisoning with sodium-channel blocking agents (e.g. tricyclic antidepressants)
  • Pre-excitation (i.e. Wolff-Parkinson-White syndrome)
  • Ventricular pacing
  • Hypothermia
  • Intermittent aberrancy (e.g. rate-related aberrancy)

Example of a Broad Complex Rhythm:

Ventricular tachycardia: Broad QRS complexes with no visible P waves. 



Ventricular vs supraventricular rhythms

Differentiation between ventricular complexes and aberrantly conducted supraventricular complexes may be difficult.

  • In general, aberrant conduction of sinus rhythm and atrial rhythms (tachycardia, flutter, fibrillation) can usually be identified by the presence of preceding atrial activity (P waves, flutter waves, fibrillatory waves).
  • However, aberrantly conducted junctional (AV nodal) complexes may appear identical to ventricular complexes as both produce broad QRS without any preceding atrial activity.
  • In the case of ectopic beats, this distinction is not really important (as occasional ectopic beats do not usually require treatment).
  • However, in the case of sustained tachyarrhythmias, the distinction between ventricular tachycardia and SVT with aberrancy becomes more important

Fortunately, many causes of broad QRS can be identified by pattern recognition:

  • Right bundle branch block produces an RSR’ pattern in V1 and deep slurred S waves in the lateral leads.
  • Left bundle branch block produces a dominant S wave in V1 with broad, notched R waves and absent Q waves in the lateral leads.
  • Hyperkalaemia is associated with a range of abnormalities including peaked T waves
  • Tricyclic poisoning is associated with sinus tachycardia and tall R’ wave in aVR
  • Wolff-Parkinson White syndrome is characterised by a short PR interval and delta waves
  • Ventricular pacing will usually have visible pacing spikes
  • Hypothermia is associated with bradycardia, long QT, Osborn waves and shivering artefact

Low Voltage

The QRS is said to be low voltage when:

  • The amplitudes of all the QRS complexes in the limb leads are < 5 mm; or
  • The amplitudes of all the QRS complexes in the precordial leads are  < 10 mm

Electrical Alternans

  • This is when the QRS complexes alternate in height.
  • The most important cause is massive pericardial effusion, in which the alternating QRS voltage is due to the heart swinging back and forth within a large fluid-filled pericardium.

High Voltage

  • Increased QRS voltage is often taken to infer the presence of left ventricular hypertrophy.
  • However, high left ventricular voltage (HLVV) may be a normal finding in patients less than 40-45 years of age, particularly slim or athletic individuals.
  • There are multiple “voltage criteria” for left ventricular hypertrophy.
  • Probably the most commonly used are the Sokolov-Lyon criteria (S wave depth in V1 + tallest R wave height in V5-V6 > 35 mm).
  • Voltage criteria must be accompanied by non-voltage criteria to be considered diagnostic of left ventricular hypertrophy.

Spot Diagnoses

These cardiac diseases produce distinctive QRS morphologies that are important not to miss:

  • Brugada syndrome (partial RBBB with ST elevation in V1-2)
  • Wolff-Parkinson White Syndrome (delta wave)
  • Tricyclic poisoning (wide QRS with dominant R wave in aVR)


Left Atrial Enlargement

AKA: Left atrial hypertrophy, left atrial abnormality.

  • Left atrial enlargement (LAE) is due to pressure or volume overload of the left atrium.
  • It is often a precursor to atrial fibrillation.

Electrocardiographic Criteria

LAE produces a broad, bifid P wave in lead II (P mitrale) and enlarges the terminal negative portion of the P wave in V1.

Diagnostic criteria:

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


In isolation:

  • Classically seen with mitral stenosis

In association with left ventricular hypertrophy:

  • Systemic hypertension
  • Aortic stenosis
  • Mitral incompetence
  • Hypertrophic cardiomyopathy


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


P wave terminal portion > 40 ms duration in V1



P waves with terminal portion > 1mm deep in V1 



Right Atrial Enlargement

Right atrial hypertrophy, right atrial abnormality:

Electrocardiographic Criteria

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


The principal cause is pulmonary hypertension due to:

  • Chronic lung disease (cor pulmonale)
  • Tricuspid stenosis
  • Congenital heart disease (pulmonary stenosis, Tetralogy of Fallot)
  • Primary pulmonary hypertension


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



Right atrial enlargement: P wave amplitude > 1.5 mm in V2



Biatrial Enlargement


Biatrial enlargement is diagnosed when criteria for both right and left atrial enlargement are present on the same ECG.
The spectrum of P-wave changes in leads II and V1 with right, left and bi-atrial enlargement is summarised in the following diagram:



Electrocardiographic Criteria

The diagnosis of biatrial enlargement requires criteria for LAE and RAE to be met in either lead II, lead V1 or a combination of leads.

In lead II

Bifid P wave with:

  • Amplitude ≥  2.5mm


  • Duration  ≥ 120 ms

In V1

Biphasic P waves with:

  • Initial positive deflection  ≥ 1.5mm tall


  • Terminal negative deflection ≥ 1mm deep


  • Terminal negative deflection ≥ 40 ms duration

Combination criteria 

  • P wave positive deflection  ≥ 1.5 mm in leads V1 or V2


  • Notched P waves with duration >120 ms in limb leads, V5 or V6


Combination of both left and right atrial enlargement.Right atrial enlargement

  • Pulmonary hypertension due to:
  • Chronic lung disease (cor pulmonale)
  • Tricuspid stenosis
  • Congenital heart disease (pulmonary stenosis, Tetralogy of Fallot)
  • Primary pulmonary hypertension

Left Atrial Enlargement

  • Mitral valve disease
  • Aortic valve disease
  • Hypertension
  • Aortic stenosis
  • Mitral incompetence
  • Hypertrophic cardiomyopathy (HOCM)

Example ECGs

Example 1


Biatrial enlargement due to idiopathic cardiomyopathy:

Example 2


Biatrial enlargement:



EMQ wersja dla Opiekuna

Jak punktować odpowiedzi:


EMQ wersja dla Opiekuna

Jak punktować odpowiedzi:


EMQ wersja dla Opiekuna

Jak punktować odpowiedzi:


Baza wyników

Plik emq.html zostanie zapisany w katalogu głównym urządzenia (dostępnym bez konieczności rootowania). Będzie on zawierał wszystkie zapisane dane: ID, wiek, wersję testu, wynik sumaryczny, odpowiedzi na poszczególne pytania, datę.



If you are a cardiologist in practice, a fellow in training, medical student, or a anesthesiologist, then this is the right place to help you learn and review principles of ECG..

Developed By

Disclaimer: This information on this site is meant to be purely educational and in no way should substitute for clinical judgment or be used as a means to make decisions regarding clinical care.Special thanks for Ed Burns

Powered by: jQuery Mobile |