ECG Rate


ECG Rate

  • The usual paper speed is 25mm/sec
  • 1mm (small square) = 04 sec
  • 5mm (big square) = 0.2 sec
  • Calculate atrial and ventricular rates separately if they are different (e.g. complete heart block).
  • For regular rhythms:  Rate = 300 / number of large squares in between each consecutive R wave. (MCQ)
  • For very fast rhythms:  Rate = 1500 / number of small squares in between each consecutive R wave. (MCQ)
  • For slow or irregular rhythms:  Rate = number of complexes on the rhythm strip x 6  (this gives the average rate over a ten-second period).
  • Interpretation (adults)
    • 60–100 beats/min -Normal
    • >100 beats/min -Tachycardia
    • <60 beats/min –Bradycardia
  • Normal Heart Rates in Children (MCQ)
    • Newborn: 110 – 150 bpm
    • 2 years: 85 – 125 bpm
    • 4 years: 75 – 115 bpm
    • 6 years+: 60 – 100 bpm


ECG Rhythm

Rhythm strip – On a 12 lead ECG this is usually a 10 second recording from Lead II.

A useful 7 step approach to rhythm analysis

  1. Rate —
    1. Tachycardia or bradycardia?
    2. Normal rate is 60-100/min.
  2. Pattern of QRS complexes —
    1. Regular or irregular?
    2. If irregular is it regularly irregular or irregularly irregular?
  3. QRS morphology —
    1. Narrow complex — sinus, atrial or junctional origin.
    2. Wide complex — ventricular origin, or supraventricular with aberrant conduction.
  4. P waves —
    1. Absent — sinus arrest, atrial fibrillation
    2. Present — morphology and PR interval may suggest sinus, atrial, junctional or even retrograde from the ventricles.
  5. Relationship between P waves and QRS complexes —
    1. AV association (may be difficult to distinguish from  isorhythmic dissociation)
    2. AV dissociation
      1. complete — atrial and ventricular activity is always independent.
      2. incomplete — intermittent capture.
    3. Onset and termination —
      1. Abrupt — suggests re-entrant process.
      2. Gradual — suggests increased automaticity.
    4. Response to vagal manoeuvres —
      1. Sinus tachycardia, ectopic atrial tachydysrhythmia — gradual slowing during the vagal manoeuvre, but resumes on cessation.
      2. AVNRT or AVRT — abrupt termination or no response.
      3. Atrial fibrillation and atrial flutter — gradual slowing during the manoeuvre.
      4. VT — no response.
Narrow Complex (Supraventricular) Tachycardias
Narrow Complex (Supraventricular) Tachycardias
  • Broad Complex Tachycardias
    • Regular
      • Ventricular tachycardia
      • Antidromicatrioventricular re-entry tachycardia (AVRT).
      • Any regular supraventricular tachycardia with aberrant conduction — e.g. due to bundle branch block, rate-related aberrancy.
    • Irregular 
      • 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.
    • All regular BCTs should be considered to be VT until proven otherwise.( MCQ)
  • Bradycardias
    • 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

ECG Axis

  • the mean direction of electrical forces in the frontal plane ( limb leads) as measured from the zero reference point (lead 1)
  • Normal values
    • P wave: 0 to 75 degrees
    • QRS complex: -30 to 90 degress
    • T wave: QRS-T angle <45 degrees frontal or <60 degrees precordial



  • Quick look tests
  • The simplest method of identifying gross deviations in axis is to look at the QRS complexes in leads I and aVF.
    • Lead I is a left-sided lead, and as aVF is perpendicular to lead I, it can be considered a right-sided lead.
    • Both leads I and aVF have mainly positive QRS complexes = normal axis.
    • Lead I is positive and aVF is negative = left axis deviation (LAD).
    • Lead I is negative and aVF is positive = right axis deviation (RAD).
  • Both leads negative = extreme RAD or “North-West” axis

QRS Deflection


QRS Deflection 2
QRS Deflection 2


  • Interpretation of QRS Axis
  • Normal
    • 0 to 90 degrees
  • Right Axis Deviation (RAD)
    • > 90 degrees
      • moderate RAD: 90 to 120 degrees
      • marked RAD: 120 to 180 degrees
    • Differential diagnosis
      • Right Ventricular Hypertrophy (RVH) — most common
      • Left Posterior Fascicular Block (LPFB) — diagnosis of exclusion
      • Lateral and apical MI
      • Acute Right Heart Strain, e.g. acute lung disease such as pulmonary embolus
      • Chronic lung disease, e.g. COPD
      • Dextrocardia
      • Ventricular pre-excitation (WPW) — LV free wall accessory pathway
      • Ventricular ectopy
      • Hyperkalemia
      • Sodium-channel blockade, e.g. tricyclic toxicity
      • Secundum ASD — rSR’ pattern
      • Normal in infants and children
      • Normal young or slender adults with a horizontally positioned heart can also
demonstrate a rightward QRS axis on the ECG.
    • Left Axis Deviation (LAD)
      • <-30 degrees
        • moderate LAD: -30 to -45 degrees
        • marked LAD: -45 to -90 degrees
      • Differential diagnosis
        • Left ventricular hypertrophy (LVH)
        • Left Anterior Fascicular Block (LAFB) — diagnosis of exclusion
        • LBBB
        • inferior MI
        • ventricularectopy
        • paced beats
        • Ventricular pre-excitation (WPW)
        • Primum ASD — rSR’ pattern
      • Extreme Axis Deviation
        • 180 to -90 degrees – rare
        • Differential diagnosis
          • Right Ventricular Hypertrophy (RVH)
          • Apical MI
          • VT
          • Hyperkalemia


    • can be thought of as the axis of the heart in the transverse axis (the precordial leads)
    • Normal
      • isoelectric QRS in V3 and V4, indicating the transition point between the right and left ventricular electric forces
    • Clockwise rotation
      • isoelectric QRS in V5, V6
    • Anti-clockwise rotation
      • isoelectric QRS in V1, V2
    • Rule of thumb: the heart rotates towardshypertropy and away from infarction
    • 12 Lead ECG

– 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)

The P wave

  • The P wave is the first positive deflection on the ECG
  • It represents atrial depolarization
  • Characteristics of the Normal Sinus P Wave
  • Morphology
    • Smooth contour
    • Monophasic in lead II
    • Biphasic in V1
  • Axis
    • Normal P wave axis is between 0° and +75°
    • P waves should be upright in leads I and II, inverted in aVR
  • Duration – < 120 ms
  • Amplitude
    • < 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 depolarisationlasts longer than normal and its waveform extends to the end of left atrial depolarisation.
  • Although the amplitude of the right atrial depolarisationcurrent 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.



Normal p wave in v1
Normal p wave in v1


  • Right Atrial Enlargement – Lead V1
  • Right atrial enlargement causes increased height (> 1.5mm) in V1 of the initial positive deflection of the P wave.
right ventricular hypertrophy
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.



ecg left
ecg left
  • 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:


p wave changes
p wave changes


  • 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.
P mitrale
P mitrale


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. corpulmonale from chronic respiratory disease).

P Pulmonale
P Pulmonale


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
accelerated junctional 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
multifocal atrial rhythm


multifocal atrial tachycardia
multifocal atrial tachycardia


  • The Q wave
    • A Q wave is any negative deflection that precedes an R wave
    • 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) width
        • > 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
      • 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

  • 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
  • Causes of Dominant R wave in 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)
    • Poisoning with sodium-channel blocking drugs
      • Causes a characteristic dominant terminal R wave in aVR
      • Poisoning with sodium-channel blocking agents is suggested if:
        • R wave height > 3mm
        • R/S ratio > 0.7
      • Dextrocardia
        • ECG shows all the classic features of dextrocardia:
          • Positive QRS complexes (with upright P and T waves) in aVR
          • Negative QRS complexes (with inverted P and T waves) in lead I
          • Marked right axis deviation
          • Absent R-wave progression in the chest leads (dominant S waves throughout)
        • Left arm/right arm lead reversal
          • 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.
          • Note that absent R wave progression is characteristically seen in dextrocardia
          • With LA/RA lead reversal
            • Lead I becomes inverted
            • Leads aVR and aVL switch places
            • Leads II and III switch places
          • 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


T Wave

  • The T wave is the positive deflection after each QRS complex.
  • It represents ventricular
  • Characteristics of the normal T wave
    • Upright in all leads except aVR and V1
    • Amplitude < 5mm in limb leads, < 15mm in precordial leads
  • 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
  • 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.
  • Loss of precordial T-wave balance
    • Loss of precordial T-wave imbalance occurs when the upright T wave is larger than that in V6.
    • This is a type of hyperacute T wave.
    • The normal T wave in V1 is inverted.
    • An upright T wave in V1 is considered abnormal — especially if it is tall (TTV1), and especially if it is new (NTTV1).
    • This finding indicates a high likelihood of coronary artery disease, and when new implies acute ischemia.
  • 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.
  • 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.
  • Myocardial Ischaemia and Infarction
    • T-wave inversions due to myocardial ischaemia or infarction occur in contiguousleads based on the anatomical location of the area of ischaemia/infarction:
      • Inferior =  II, III, aVF
      • Lateral =  I, aVL, V5-6
      • Anterior =  V2-6
    • Dynamic T-wave inversions are seen with acute myocardial ischaemia.
    • Fixed T-wave inversions are seen following infarction, usually in association with pathological Q waves.
  • Bundle Branch Block
    • Left Bundle Branch Block
    • Right Bundle Branch Block
    • 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.
      • 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).
      • 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.
        • 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).
      • Hypertrophic Cardiomyopathy (HOCM)
        • HOCM is associated with deep T wave inversions in all the precordial leads.
      • Raised intracranial pressure
        • Events causing a sudden rise in ICP (e.g. subarachnoid haemorrhage) produce widespread deep T-wave inversions with a bizarre morphology.
      • Biphasic T waves
        • There are two main causes of biphasic T waves:
        • The two waves go in opposite directions:
          • Ischaemic T waves go up then down
          • Hypokalaemic T waves go down then up
        • 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
          • ‘Camel hump’ T waves
            • Used 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
            • 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).
              • Ischaemia
                • Dynamic T-wave flattening due to anterior ischaemia
                • T waves return to normal once the ischaemia resolves
              • Hypokalaemia
                • Note generalised T-wave flattening with prominent U waves in the anterior leads (V2 and V3).

The 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.
  • Source of the U wave
    • The source of the U wave is unknown.
    • Three common theories regarding its origin are:
      • Delayed repolarisation of Purkinje fibres
      • Prolonged repolarisation of mid-myocardial “M-cells”
      • After-potentials resulting from mechanical forces in the ventricular wall
    • 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
    • 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 withschest 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


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


  • Short PR interval (< 120ms)
  • Broad QRS (> 100ms)
  • A slurred upstroke to the QRS complex (the delta wave)
  • Osborn Wave (J Wave)
    • The Osborn wave (J wave) is a positive deflection at the J point (negative in aVR and V1)
    • It is usually most prominent in the precordial leads
    • Causes
      • 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)
    • In Hypothermia ,theheight of the J wave is roughly proportional to the degree of hypothermia
  • Epsilon Wave
    • The epsilon wave is a small positive deflection (‘blip’) buried in the end of the QRS complex.
    • It is the characteristic finding in arrhythmogenic right ventricular dysplasia (ARVD).
    • 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)
      • LocalisedQRS widening of 110ms in V1-3
      • Paroxysmal episodes of ventricular tachycardia with a LBBB morphology

 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
      • The normal PR interval is between 120 – 200 ms duration (three to five small squares).
      • If the PR interval is > 200 ms,first degree heart block is said to be present.
      • PR interval < 120 ms suggests pre-excitation (the presence of an accessory pathway between the atria and ventricles) or AV nodal (junctional) rhythm.
    • First degree 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)
    • Short PR interval (<120ms)
      • A short PR interval is seen with:
      • 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
      • 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.
      • 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).

The 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
  • The characteristic changes of acute pericarditis are:
    • PR segment
    • Widespread concave (‘saddle-shaped’) ST elevation.
    • Reciprocal ST depression and PR elevation in aVR and V1
    • Absence of reciprocal ST depression
  • PR segment changes are relative to the baseline formed by the T-P segment.

J point

  • The J point is the the junction between the termination of the QRS complex and the beginning of the ST segment.
  • Abnormalitites

QRS Complex

  • 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).
    • 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)
    • 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)
    • Ventricular tachycardia: Broad QRS complexes with no visible P waves.
      • Fortunately, many causes of broad QRS can be identified by pattern recognition:
      • 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.


  • QT Interval
    • The QT interval is the time from the start of the Q wave to the end of the T wave.
    • It represents the time taken for ventricular depolarisation and repolarisation
    • 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.
    • The QT interval should be measured in either lead II or V5-6
    • 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.
      • Bazett’s formula: QTC = QT / √ RR
      • 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.
    • 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
      • Hypokalaemia causes apparent QTc prolongation in the limb leads (due to T-U fusion) with prominent U waves in the precordial leads.
    • Hypocalcaemia
      • Hypocalcaemia typically prolongs the ST segment, leaving the T wave unchanged.
    • Hypothermia
      • Severe hypothermia can cause marked QTc prolongation, often in association with bradyarrhythmias (especially slow AF), Osborne waves and shivering artifact.
    • Myocardial Ischaemia
    • Raised ICP
      • A sudden rise in intracranial pressure (e.g. due to subarachnoid haemorrhage) may produce characteristic T wave changes (‘cerebral T waves’): widespread, deep T wave inversions with a prolonged QTc.
    • Congenital Long QT Syndrome
      • There are several congenital disorders of ion channels that produce a long QT syndrome and are associated with increased risk of torsades de pointes and sudden cardiac death.
    • Causes of a short QTc (<350ms)
    • Hypercalcaemia
      • Hypercalcaemialeads to shortening of the ST segment and may be associated with the appearance of Osborne waves.
    • Congenital short QT syndrome
      • Congenital short QT syndrome (SQTS) is an autosomal-dominant inherited disorder of potassium channels associated with an increased risk of paroxysmal atrial and ventricular fibrillation and sudden cardiac death.
      • The main ECG changes are very short QTc (<300-350ms) with tall, peaked T waves.
      • Short QT syndrome may be suggested by the presence of:
        • Lone atrial fibrillation in young adults
        • Family member with a short QT interval
        • Family history of sudden cardiac death
        • ECG showing QTc< 350 ms with tall, peaked T waves
        • Failure of the QT interval to increase as the heart rate slows
      • Digoxin
        • Digoxinproduces a relative shortening of the QT interval, along with downward sloping ST segment depression in the lateral leads (‘reverse tick’ appearance), widespread T-wave flattening and inversion, and a multitude of arrhythmias (ventricular ectopy, atrial tachycardia with block, sinus bradycardia, regularized AF, any type of AV block).
      • 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 absoluterather than corrected
        • 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

  • The ST segment is the flat, isoelectric section of the ECG between the end of the S wave (the J point) and the beginning of the T wave.
  • It represents the interval between ventricular depolarization and repolarization.
  • The most important cause of ST segment abnormality (elevation or depression) is myocardial ischaemia or infarction.
  • Causes of ST Segment Elevation
  • Morphology of the Elevated ST segment
    • Myocardial Infarction
    • 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
      • Pericarditis causes widespread concave (“saddleback”) ST segment elevation with PR segment depressionin 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
      • BER causes mild ST elevation with tall T-wavesmainly in the precordial leads and inferior 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
      • 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
      • This is an ECG pattern of residual ST elevation and deep Q waves seen in patients with previous myocardial infarction.
    • 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.
    • Ventricular Paced Rhythm
      • 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
      • 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”).
    • Less Common Causes of ST segment Elevation
    • Causes of ST Depression
    • Morphology of ST Depression
      • Myocardial Ischaemia
        • ST depression can be eitherupsloping, downsloping, or horizontal.
        • Horizontal or downsloping ST depression ≥ 0.5 mm at the J-point in ≥ 2 contiguous leadsindicates myocardial ischaemia (according to the 2007 Task Force Criteria).
        • Upsloping ST depression in the precordial leads with prominent “De Winter’s” T wavesis 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 due to subendocardialischaemia 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 occlusionand severe triple vessel disease.
        • ST depression localised to the inferior or high lateral leads is more likely to represent reciprocal change than subendocardialischaemia. 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 STEMIproduces reciprocal ST depression in III and aVF (± lead II).
          • Reciprocal ST depression in V1-3 occurs with posterior infarction
        • 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.
        • De Winters T Waves
          • This pattern of upsloping 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.
        • Digoxin Effect
          • Treatment with digoxin causes downsloping ST depression with a “sagging”  morphology, reminiscent of Salvador Dali’s moustache.
        • Hypokalaemia
          • 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 Bundle Branch Block
          • RBBB may produce a similar pattern of repolarisation abnormalities to RVH, with ST depression and T wave inversion in V1-3.
        • 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

Cardiac Conduction System and Understanding ECG, Animation
The cardiac conduction system consists of the following components:
– The sinoatrial node, or SA node, located in the right atrium near the entrance of the superior vena cava. This is the natural pacemaker of the heart. It initiates all heartbeat and determines heart rate. Electrical impulses from the SA node spread throughout both atria and stimulate them to contract.

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