LITFL ECG

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

• < 0.12 s (<120ms or 3 small squares)

• < 2.5 mm (0.25mV) in the limb leads

• < 1.5 mm (0.15mV) in the precordial leads

• 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.

• 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.

• 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).

• 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”).

• 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.

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 context

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

• > 40 ms (1 mm) wide

• > 2 mm deep

• > 25% of depth of QRS complex

• Seen in leads V1-3

Differential Diagnosis

• Myocardial infarction

• Cardiomyopathies — Hypertrophic (HCM), 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.

R wave Overview

Abnormalities of the R wave

1. Dominant R wave in V1

2. Dominant R wave in aVR

3. Poor R wave progression

1. 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

Wolff-Parkinson-White (WPW) Type A

Leads V1 and V3 reversed

• Note biphasic P wave (typically seen in only in V1) in lead “V3”

Muscular dystrophy

2. 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)

Examples of Dominant R wave in aVR

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

• 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

• Lead I becomes inverted

• Leads aVR and aVL switch places

• Leads II and III switch places

Ventricular Tachycardia

3. Poor R wave progression

• Prior anteroseptal MI

• LVH

• Inaccurate lead placement

• May be a normal variant

T wave Overview

• Upright in all leads except aVR and V1

• Amplitude < 5mm in limb leads, < 10mm in precordial leads (10mm in men, 8mm in women)

• Duration (see QT interval)

• Peaked T waves

• Hyperacute T waves

• Inverted T waves

• Biphasic T waves

• ‘Camel Hump’ T waves

• Flattened T waves

Peaked T waves

Hyperacute T waves

Loss of precordial T-wave balance

• 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

• 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

• 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

• 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

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

Right Bundle Branch Block

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

Ventricular Hypertrophy

Left Ventricular Hypertrophy

• Left ventricular hypertrophy (LVH) 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

• T-wave inversions in the right precordial (V1-3) and inferior (II, III, aVF) leads.

SI QIII TIII

• 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 (HCM)

• Hypertrophic Cardiomyopathy is associated with deep T wave inversions in all the precordial leads.

Raised intracranial pressure (ICP)

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

Biphasic T waves

• Myocardial ischaemia

• Hypokalaemia

Wellens Syndrome

• Type A = Biphasic T waves with the initial deflection positive and the terminal deflection negative (25% of cases)

• Type B = T-waves are deeply and symmetrically inverted (75% of cases)

Wellens Type A

• Wellens Pattern A (Type 1)

• Wellens Pattern A (Type 1)

Wellens Type B

• Wellens Pattern B (Type 2)

• Wellens Pattern B (Type 2)

‘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

• ischaemia (if dynamic or in contiguous leads) or

• electrolyte abnormality, e.g. hypokalaemia (if generalised).

Hypokalaemia

U wave Overview

• U wave is usually in the same direction as the T wave.

• U wave is best seen in leads V2 and V3.

Source of the U wave

• 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 wav

• 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

• >1-2mm or 25% of the height of the T wave.

• Bradycardia

• Severe hypokalaemia.

• Hypocalcaemia

• Hypomagnesaemia

• Hypothermia

• Raised intracranial pressure

• Left ventricular hypertrophy

• Hypertrophic cardiomyopathy

• Digoxin

• Phenothiazines (thioridazine)

• Class Ia antiarrhythmics (quinidine, procainamide)

• Class III antiarrhythmics (sotalol, amiodarone)

Prominent U waves due to sinus bradycardia

U waves associated with hypokalaemia

U waves associated with left ventricular hypertrophy

U waves associated with digoxin use

U waves associated with quinidine use

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

• Coronary artery disease

• Hypertension

• Valvular heart disease

• Congenital heart disease

• Cardiomyopathy

• Hyperthyroidism

• 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

Unstable angina

• Inverted U waves in a patient with unstable angina. Reproduced from Girish et al.

Inverted U waves in Prinzmetal angina

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.

Osborn Wave (J Wave) Overview

• The ECG finding of a positive deflection at the J point (negative in aVR and V1) with a dome or hump configuration is most frequently termed a J wave or Osborn wave.

• No definitive physiological cause for the deflection despite numerous postulates.

• Broad differential diagnosis of prominent Osborn waves including hypothermia; benign early repolarization; hypercalcaemia and the Brugada syndrome.

• In the setting of hypothermia this phenomenon is most commonly referred to as an Osborn wave. Compared to other hypothermia-induced ECG abnormalities (e.g. sinus bradycardia; supraventricular arrhythmias, QT prolongation and AV block) the Osborn wave is thought to be the most specific

• Normal variant

• Hypercalcaemia

• Medications

• Neurological insults such as intracranial hypertension, severe head injury and subarachnoid haemorrhage

• Le syndrome d’Haïssaguerre (idiopathic VF)

Delta Wave Overview

• Short PR interval (< 120ms)

• Broad QRS (> 100ms)

• A slurred upstroke to the QRS complex (the delta wave)

ECG examples of Delta Waves

• Delta wave

• Delta wave

• Delta wave

• Negative delta wave

• Negative delta wave



 
 

Epsilon Wave Definition

The epsilon wave is a small positive deflection (‘blip’ or ‘wiggle’) buried in the end of the QRS complex. Epsilon waves are caused by postexcitation of the myocytes in the right ventricle.
Epsilon waves are the most characteristic finding in arrhythmogenic right ventricular dysplasia (ARVD/C). Here myocytes are replaced with fat, producing islands of viable myocytes in a sea of fat. This causes a delay in excitation of some of the myocytes of the right ventricle and causes the little wiggles seen during the ST segment of the ECG.
Epsilon waves have also been described in patients with posterior myocardial infarction; right ventricular infarction; infiltration disease, and sarcoidosis.
Epsilon waves are best seen in the ST segments of leads V1 and V2, and most commonly seen in leads V1 through V4.
 

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.
• The normal PR interval is between 120 – 200 ms (0.12-0.20s) in 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.



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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)

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First degree AV block



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

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



• Second degree heart block, Mobitz type I (Wenckebach 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).

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Short PR interval (<120ms)

A short PR interval is seen with:
• Preexcitation syndromes
• AV nodal (junctional) rhythm.

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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.

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Wolff-Parkinson-White syndrome

The characteristic features of Wolff-Parkinson-White syndrome are a short PR interval (<120ms), broad QRS and a slurred upstroke to the QRS complex, the delta wave.



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Lown-Ganong-Levine syndrome

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



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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).
• ECG: Accelerated junctional rhythm demonstrating inverted P waves with a short PR interval (retrograde P waves)



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

These occur in two main conditions:
• Pericarditis
• Atrial ischaemia

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Pericarditis

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.



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

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

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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.

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Liu’s criteria for diagnosing atrial ischaemia / infarction include:
• PR elevation >0.5 mm in V & V with reciprocal PR depression in V & V
5
6
1
2
• 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)

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PR depression in inferior STEMI indicating concomitant atrial infarction



Profound PR-segment depression in inferior leads: (A) with clear-cut TP segment; and (B) without clear-cut TP segment; in acute inferior myocardial infarction. Note also ST-segment elevation in inferior leads. (Reproduced from Jim et al.)

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Measurement of PR depression



• Measurement of PR-segment depression: (A) with clear-cut TP segment; and (B) without clear-cut TP segment. (Reproduced from Jim et al.)
 

The Q-T 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, effectively the period of ventricular systole from ventricular isovolumetric contraction to isovolumetric relaxation



The QT interval is inversely proportional to heart rate:

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

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How to measure the QT interval

• 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

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Corrected QT interval (QTc)

• The corrected QT interval (QTc) estimates the QT interval at a standard 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 formula: QT = QT / √ RR
C
• Fridericia formula: QT = QT / RR
C
1/3
• Framingham formula: QT = QT + 0.154 (1 – RR)
C
• Hodges formula: QT = QT + 1.75 (heart rate – 60)
C
Note: The RR interval is given in seconds (RR interval = 60 / heart rate).
• Bazett and Fridericia are logarithmic corrections whereas Hodges and Framingham are linear correction formulae.
• Henry Cuthbert Bazett derived his formula in 1920. Bazett 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.
• Louis Sigurd Fridericia derived his formula in 1920 from 50 health individuals aged between 3 and 81 years old. Fredericia formula is the observed QT interval divided by cube root of RR interval, in seconds.
• Charbit B et al in a study of 108 patients found that automatic QT correction using Bazett formula had a sensitivity for detection of QT prolongation of 54% while automatic QT correction using Fridericia formula had 100% sensitivity.
• 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!
Fortunately, there are now multiple i-phone apps that will calculate QTc for you (e.g. MedCalc), and the website MDCalc.com has a quick and easy QTc calculator that is free to use.

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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

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Causes of a prolonged QTc (>440ms)

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

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Hypokalaemia



• Apparent QTc 500ms – prominent U waves in precordial leads (hypokalaemia (K+ 1.9))
• Hypokalaemia causes apparent QTc prolongation in the limb leads (due to T-U fusion) with prominent U waves in the precordial leads.

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Hypomagnesaemia



• QTc 510 ms secondary to hypomagnesaemia

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Hypocalcaemia



• QTc 510ms due to hypocalcaemia
• Hypocalcaemia typically prolongs the ST segment, leaving the T wave unchanged.

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Hypothermia



• QTc 620 ms due to severe hypothermia
• Severe hypothermia can cause marked QTc prolongation, often in association with bradyarrhythmias (especially slow AF), Osborn waves and shivering artefact.

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Myocardial Ischaemia



• QTc 495 ms due to hyperacute MI
• Myocardial ischemia tends to produce a modest increase in the QTc, in the 450-500 ms range.
• This may be useful in distinguishing hyperacute MI from benign early repolarization (both may produce similar hyperacute T waves, but benign early repolarisation (BER) will usually have a normal QTc).

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Raised ICP



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

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Congenital Long QT Syndrome



• QTc 550ms due to 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.

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Causes of a short QTc (<350ms)

• Hypercalcaemia
• Congenital short QT syndrome
• Digoxin effect

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Hypercalcaemia



• Marked shortening of the QTc (260ms) due to hypercalcaemia
• Hypercalcaemia leads to shortening of the ST segment and may be associated with the appearance of Osborne waves.

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Congenital short QT syndrome



• Very short QTc (280ms) with tall, peaked T waves due to 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.

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



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Digoxin

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



Digoxin produces 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).

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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):



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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 (developed by Chan et al) to determine whether the patient is at risk of TdP.
• The QT nomogram is a clinically relevant risk assessment tool that predicts arrhythmogenic risk for drug-induced QT prolongation can be used for risk stratification
• A QT interval-heart rate pair that plots above the line indicates the patient is at risk of TdP.



 

S-T 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.
• The ST Segment represents the interval between ventricular depolarization and repolarization.
• The most important cause of ST segment abnormality (elevation or depression) is myocardial ischaemia or infarction.



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Causes of ST Segment Elevation
• Acute myocardial infarction
• Coronary vasospasm (Printzmetal’s angina)
• Pericarditis
• Benign early repolarization
• Left bundle branch block
• Left ventricular hypertrophy
• Ventricular aneurysm
• Brugada syndrome
• Ventricular paced rhythm
• Raised intracranial pressure
• Takotsubo Cardiomyopathy

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Morphology of the Elevated ST segment
Myocardial Infarction



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

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ST Segment Morphology in Other Conditions





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Patterns of ST Elevation

Acute ST elevation myocardial infarction (STEMI)

ST segment elevation and Q-wave formation in contiguous leads. Follow the links above to find out more about the different STEMI patterns.:
• Septal (V1-2)
• Anterior (V3-4)
• Lateral (I + aVL, V5-6)
• Inferior (II, III, aVF)
• Right ventricular (V1, V4R)
• Posterior (V7-9)

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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).



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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.

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Pericarditis

Acute 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.



• Concave “saddleback” ST elevation in leads I, II, III, aVF, V5-6 with depressed PR segments.
• There is reciprocal ST depression and PR elevation in leads aVR and V1.
• Spodick’s sign was first described by David H. Spodick in 1974 as a downward sloping TP segment with specificity for acute pericarditis.

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Benign Early Repolarization

Benign Early Repolarization (BER) causes mild ST elevation with tall T-waves mainly in the precordial leads. BER 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.



There is slight concave ST elevation in the precordial and inferior leads with notching of the J-point (the “fish-hook” pattern)

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Left Bundle Branch Block (LBBB)

In Left bundle branch block (LBBB), 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).



• Note the ST elevation in leads with deep S waves — most apparent in V1-3.
• Also note the ST depression in leads with tall R waves — most apparent in I and aVL.

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Left Ventricular Hypertrophy (LVH)

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).



• Deep S waves with ST elevation in V1-3
• ST depression and T-wave inversion in the lateral leads V5-6
• Note in this this case there is also right axis deviation, which is unusual for LVH and may be due to associated left posterior fascicular block.

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Ventricular Aneurysm

This is an ECG pattern of Ventricular Aneurysm – 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.



• There is ST elevation with deep Q waves and inverted T waves in V1-3.
• This pattern suggests the presence of a left ventricular aneurysm due to a prior anteroseptal MI.

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Brugada Syndrome

Brugada Syndrome is 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”.

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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.



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Raised Intracranial Pressure

Raised Intracranial Pressure (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.

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Takotsubo Cardiomyopathy

Takotsubo Cardiomyopathy: A STEMI mimic producing ischaemic chest pain, ECG changes +/- elevated cardiac enzymes with characteristic regional wall motion abnormalities on echocardiography.
Typically occurs in the context of severe emotional distress (“broken heart syndrome“). Commonly associated with new ECG changes (ST elevation or T wave inversion) or moderate troponin rise.



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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

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Transient ST elevation after DC cardioversion from VF



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J waves in hypothermia simulating ST elevation



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Causes of ST Depression

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

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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 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.

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ST Segment depression



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ST segment morphology in myocardial ischaemia



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Reciprocal change



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ST segment morphology in posterior MI



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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.



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. This concept is discussed further here.

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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

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• Reciprocal ST depression in III and aVF with high lateral STEMI

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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.



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De Winter T Waves

De Winter T waves: a 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.



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Digoxin Effect

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



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Hypokalaemia

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



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Right ventricular hypertrophy (RVH)

Right ventricular hypertrophy (RVH) causes ST depression and T-wave inversion in the right precordial leads V1-3.



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Right Bundle Branch Block (RBBB)

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.



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Supraventricular tachycardia (SVT)
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.





 
The J point
The J point is the the junction between the termination of the QRS complex and the beginning of the ST segment.
The J (junction) point marks the end of the QRS complex, and is often situated above the baseline, particularly in healthy young males.
On most ECGs the determination of the J point as a demarcation between QRS and the start of the ST is clear. However with the advance of electrophysiological studies and scrutiny of the cellular/ionic mechanisms at each stage of the ECG – these lines become blurred.
For simplicity:
• J point is present in all ECGs and marks the transition of QRS complex to ST segment
• J wave deflection occurs before the J point
• The position of the J point in relation to a slurred terminal QRS is still debated.
J point in a) normal; b) c) J point elevation; d) J point depression; e) with J wave (Osborn wave)



Note: The letter J on the ECG defines 2 totally different and unrelated events. The J point is a point in time marking the end of the QRS and the onset of the ST segment present on all ECG’s; the J wave is a much less common long slow deflection of uncertain origin originally described in relation to hypothermia.
Abnormalities of the J point
• Elevation or depression of the J point is seen with the various causes of ST segment abnormality. It may be elevated as a result of injury currents during acute myocardial ischemia and pericarditis, as well as in various other patterns of both normal and abnormal ECGs
• Elevation of the J point occurs with benign early repolarisation
• A positive deflection prior to the J point is termed a J wave (Osborn wave) and is characteristically seen with hypothermia.



 
QRS Complex Morphology
Main Features to Consider
• Width of the complexes: Narrow versus broad.
• Voltage (height) of the complexes.
• Spot diagnoses: Specific morphology patterns that are important to recognise.

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QRS Complex Naming Convention



Courtesy of ECGwaves.com
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 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.

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Narrow QRS Complex Morphology
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.



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



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



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Broad QRS Complex Morphology
Broad/Wide QRS 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 (RBBB or LBBB)
• 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.

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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. This topic is covered in more detail here.

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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

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High Voltage QRS Morphology
• 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.

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Low Voltage QRS Morphology
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

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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.
 
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)