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Syncope ECGs


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In the previous post we learnt that although cardiac syncope is rare, it is potentially fatal. It is, therefore, essential that we know how to recognise ECGs that identify the cause of cardiac syncope. Here we discuss some of the more common variants…

This post is part of our Syncope Sunday series – you can read the other posts: Post 1 – what is syncope?; Post 2 – reflex syncope; Post 3 – cardiac syncope.

Hypertrophic obstructive cardiomyopathy

HOCM is the leading cause of SADS in young athletes. It involves myocardial hypertrophy of the nondilated left ventricle. There is impaired filling, especially at times of stress with electrical disruption and variable outflow obstruction.

HOCM is worse on exercise. 55% have a family history


  • High left ventricular voltage with associated ST segment / T-wave abnormalities
  • Deep, narrow (“dagger-like”) Q waves in the lateral(I aVL V5 V6) > inferior leads – not had a previous lateral MI and not in LVH – not sensitive but is specific
  • Left atrial enlargement – bifid p waves

Arrhythmogenic right ventricular cardiomyopathy

AKA arrhythmogenic right ventricular dysplasia (ARVD)

AVRC was first described in 1978 and has autosomal dominant inheritance.

Fibro fatty replacement of right ventricle leads to a dilated and hypokinetic right ventricle and, if undetected, death.

It is the second most common cause of SADS.

Patients have palpitations, syncope and cardiac arrest.

The ECG is difficult to interpret.


  • Epsilon wave (most specific finding, seen in 30% of patient) – notch at end of QRS complex
  • T wave inversions in V1-3 (85% of patients)
  • Prolonged S-wave upstroke V1-3 (95% of patients)
  • Localised QRS widening of 110ms in V1-3

Wolff-Parkinson-White syndrome


  • Sinus rhythm with a very short PR interval
  • Broad QRS complexes with a slurred upstroke to the QRS complex — the delta wave
  • Tall R waves and inverted T waves in V1-3 mimicking right ventricular hypertrophy — these changes are due to WPW and do not indicate underlying RVH
  • Negative delta wave in aVL simulating the Q waves of lateral infarction — this is referred to as the “pseudo-infarction” pattern.

Brugada syndrome

This is autosomal dominant with variable penetrance and is a sodium channelopathy. There is an association with long QT syndrome. It more commonly presents with VF, but syncope is well documented.

1. Adult study of 104 symptomatic patients with ECG changes: 73% VF, 27% syncope

2. 30 adult patients with ECG changes: 44% syncope, 56% arrest of which 82% had a history of syncope


Brugada type 1



There are various ECG patterns:

  • Coved ST segment elevation >2mm in >1 of V1-V3 followed by a negative T wave) is the only ECG abnormality that is potentially diagnostic.

brugada sign

This above ECG sign is referred to as the Brugada sign.


Brugada type 2


  • Brugada type 2 – >2mm of saddleback shaped ST elevation


Brugada type 3


  • Brugada type 3 can be the morphology of either type 1 or type 2, but with <2mm of ST segment elevation.

As we can see, there are several variations of Brugada.

Consider Brugada if there are any ST abnormalities in V1-3 in a younger patient

It can look like right bundle branch block

ECG changes may be intermittent

Long QTc

These days, most ECG machines calculate this for us, but you should know how to calculate this (QT interval divided by the square root of the R-R interval).


Pediatric Electrophysiology Society Study (published in American Heart Association in 1993) describes presenting clinical features of LQTS in 287 patients from 26 centres < 21 years of age, with either documented LQTc or a family history of long QTc or a family history of unexplained syncope/seizures/cardiac arrest.

  • Mean age presentation 6.8 years
  • 61% symptomatic at presentation
  • 26% syncope
  • 10% seizures (misdiagnosed)
  • Only 9% with cardiac arrest

Of the 61% with symptoms

  • 67% with exercise
  • 18% with emotion and exercise
  • Family history positive for long QT in 39% and for sudden death in 31%

Catecholaminergic Polymorphic Ventricular Tachycardia (CPTV)

  • Mean age of presentation 6 – 10 years
  • Provoked by surge in adrenaline
  • Present with exercise or emotion induced syncope or cardiac arrest
  • Had a “fit” when woken by alarm clock
  • Often went dizzy & light headed watching a scary movie
  • Clinical diagnosis based on history around exercise/emotion induced symptoms

Early study in 1995: 21 children with CPTV:

  • Mean age of syncope 7.8 years
  • Mean age of diagnosis 9.9 years
  • 50% of the cases had initially been misdiagnosed as epilepsy and treated accordingly

So with syncope, there should be the normal ECG interpretation process but with pattern recognition awareness:

  • Brugada pattern
  • WPW delta wave
  • QT measurement
  • High left ventricular voltage and Q waves
  • Epsilon wave
  • Arrhythmias

About the authors

  • Elayne Forbes is a Paediatric Emergency Fellow working at Sydney Children's Hospital.


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