ECG of the Week – 15th August 2016 – Interpretation

The following ECG is from a 58 yr old male who presented following several hours of cardiac sounding chest pain. He was pain free when this ECG was recorded.

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  • 72 bpm
  • Regular

  • Normal
  • PR - Normal (140ms)
  • QRS - Normal (100ms)
  • Cove-shaped ST elevation in lead V1 (<1mm) and V2 (3mm)
  • Obliquely straight ST elevation V3 (4mm)
  • Possible ST depression leads III, aVF - difficult to see due to baseline artifact
  • P waves difficult to see due to baseline artifact - best seen in V2-3
  • T wave inversion leads aVR, aVL, V1-2
  • Brugada Syndrome
    • Type 1 Pattern
  • Given the history of central chest pain the presence of additional ACS must be considered especially given the flat ST elevation in V3 plus subtle inferior ST depression
This is challenging and I've never seen a case of Brugada plus ACS - serial ECG's and comparison with old ECG's are essential.
This patient had known Brugada and thankfully brought his old ECG from 10 yrs ago with him which showed all changes to be longstanding.

What happened ?

Interestingly the patient had been lost to cardiology follow-up and had no AICD inserted for his Type 1 Brugada. Given the typical nature of the pain the patient had a coronary angiogram which revealed no evidence of coronary artery disease and he is awaiting an AICD insertion.

Brugada Resources / Cases

We've had a case of Brugada before on ECG ot the Week here, which also prompted a 'guest editoral' post by Dr Ken Grauer which you can find here.

I've copied the Brugada overview and resource section from our previous post below.

So what is Brugada Syndrome ?

It's an inherited sodium channelopathy, associated with sudden death and syncope due to polymorphic VT and, as in our case, VF. 
Three types of ECG pattern are describe in Brugada, although only type 1 is considered diagnostic, as shown in our ECG.  

Type 1 ECG pattern:

  • Cove-shaped ST elevation of at least 2mm followed by a negative T wave in one or more of leads V1-3
In conjuction with these ECG features you need, at least, one of the following:
  • Document VF / polymorphic VT
  • Family history of sudden cardiac death at <45 years
  • Type 1 pattern ECG i n family members
  • Inducibility of VT with programmed stimulation
  • Syncope
  • Nocturnal agonal respiration
    • Attributed to self-terminating VF/polymorphic VT
The above diagnostic criteria are taken from the CSANZ (Cardiac Society of Australia and New Zealand) Guidelines for the diagnosis and management of Brugada syndrome, this document is well worth a read as it covers pathophysiology, diagnostic criteria, management, and includes examples of the type 2 and type 3 ECG patterns. 

Also check out the following great blog posts on Brugada:

What to do about it ?

As an emergency physician encountering a case of suspected / likely Brugada it's easy, phone your cardiologist. For those patients with a Brugada pattern ECG with a history of syncope, arrest, or arrhythmias, definitive treatment is an AICD insertion. The incidental Brugada pattern in the otherwise well patient is a bit more controversial, again from an Emergency Medicine perspective phone your cardiology team. The CSANZ guideline contains a nice algorithm for the diagnostic approach to Brugada and also discusses management strategies in the incidental and asymptomatic Brugada.

We should also be aware that some drugs can cause Brugada-like ECG changes and should be avoided in patients with known or suspected Brugada. For more information on what not to give go to which contains information for both clinicians and patients.

Check out these cases from Dr Smith's blog, here, and here, which illustrate Brugada-like changes secondary to drug therapy.

Avoiding certain drugs raises the question what should we give ?

The simple answer is electricity in the setting of acute arrhythmia. 
In those patients experiencing an arrythmic storm, or having repeated ICD shocks then iv isoprenaline has been proven to be useful and is recommended in the CSANZ guidelines.
For chronic prevention of arrythmia's the only oral agent shown to work is quinidine, but this is often very difficult to source. 

Ii is also worth noting that fever can unmask Brugada, due to impaired sodium channel function and aggressive management of fever should be instigated. Other potential precipitants include alcohol, hypokalaemia, cocaine, large carb meals, and very hot baths.

References / Further Reading

Life in the Fast Lane

  • Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P. ECG in Emergency Medicine and Acute Care. Elsevier Mosby 2005.

ECG of the Week – 8th August 2016 – Interpretation

The following ECG's are from an 85yr old female who presented with typical cardiac chest pain at rest. Both the ECG's were performed when the patient was pain free.

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Key features
  • Ventricular paced rhythm rate 60 bpm
  • Associated left axis deviation
  • RsR' pattern in lead V2 rather than typical deep S wave usually seen in RV pacing
  • Appropriate discordant ST / T wave changes
  • Sgarbossa negative
  • Ventricular paced rhythm
  • Morphology of leads V1-2 unusual for RV pacing as usually results in typical LBBB morphology
  • The frontal plane axis is -75 deg with a transition between leads V2-3. These features support correct RV lead placement rather than lead migration and may be seen with inappropriate lead positioning. Seen articles below.
  • CXR confirmed appropriate pacing lead position
Is RBBB morphology during right ventricular pacing always due to lead malposition ?

The short answer to this is no. There are cases in which an RBBB morphology can occur with appropriate right ventricular apical pacing.

In this case the patient had a chest x-ray which showed appropriate lead placement, for an example of RBBB morphology associated with lead malposition check out this case here.

Features which may assist in differentiating between lead malposition and correct placement are:
  • Frontal plane axis
  • Precordial transition point
  • Repositioning of leads V1-2

I would recommend the following freely available papers which both include a review of RBBB morphology during right ventricular pacing.
  • Erdogan O, Aksu F. Right bundle branch block pattern during right ventricular permanent pacing: Is it safe or not? Indian Pacing Electrophysiol J. 2007 Aug 1;7(3):187-91. PMID: 17684578   Full text here
  • Almehairi M, Baranchuk. Right Bundle Branch Block Morphology During Apical Right Ventricular Pacing. The Journal of Innovations in Cardiac Rhythm Management, 4 (2013), 1303–1304. Full text here

Click to enlarge

Key features
  • Sinus rhythm, rate ~60 bpm
  • PR prolongation
  • T wave inversion leads II, III, aVF, V4-6

The broad differentials for the changes on the serial ECGs are:

  • ACS
  • Structural Heart Disease
  • Cardiac T-wave Memory
T-wave memory is an interesting phenomenon that could explain the marked T wave changes seen on this ECG. It results in transient T wave changes following a period of abnormal ventricular conduction e.g. ventricular tachycardia, paced rhythms, intermittent bundle branch block or aberrant conduction. There is a recent paper by Vakil that is freely available (linked to below) that contains a nice overview of T-wave memory, proposed mechanisms, and a case example.The deep T wave inversion on this ECG correspond to the leads in which a negative QRS was seen in the patients paced ECG a finding consistent with T-wave memory. 

  • Vakil K, Gandhi S, Abidi KS, et al. Deep T-Wave Inversions: Cardiac Ischemia or Memory? JCvD 2014;2(2):116-118. Full text here.

The patient has negative serial troponins and underwent coronary angiography which showed irregularities only to left main, circumflex and right coronary artery.

References / Further Reading
  • Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P. ECG in Emergency Medicine and Acute Care. Elsevier Mosby 2005.

ECG of the Week – 1st August 2016 – Interpretation

The following ECG is from a 55 yr old male who presented with chest pain. He is a smoker with a history of controlled hypertension.

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  • 66 bpm
  • Sinus arrhythmia
  • Right axis deviation
  • PR - Normal (~180ms)
  • QRS - Normal (110ms)
  • QT - 400ms (QTc Bazette 420 ms)

  • ST elevation leads I (<1mm), aVL (0.5-1mm), V1 (<1mm), V2-3 (1mm)
  • ST depression lead III


  • P wave prolonged 110ms and notched in lead II consistent with left atrial abnormality
  • Poor R wave progression
  • Concordant T wave inversion leads III & aVF
  • R wave aVL ~11mm - LVH voltage criteria


  • Sinister features for ACS include concordant T wave inversion in inferior leads and concordant ST elevation in high lateral leads (I, aVL)
  • ST changes in the right precordial leads (V1-3) may be explained by LVH

What happened ?

Initial troponin was elevated at 5.69 (cTnI [<0.05 ug/L]). The patient was admitted under cardiology and had an angiogram which showed:

  • LMCA: Normal
  • LAD: 30-40% stenosis mid and distal
  • Cx: Irregularities
  • RCA: 30-40% stenosis mid vessel
  • 2nd OM: 100% occlusion with RCA collaterals - DES inserted

Post angio echo showed:

  • EF 52%
  • Hypokinesis of lateral wall of left ventricle
  • Moderate concentric left ventricular hypertrophy

The patient was discharged on dual anti-platelet therapy (DAPT), beta-blocker, statin and ACE. 

References / Further Reading

Life in the Fast Lane

  • Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P. ECG in Emergency Medicine and Acute Care. Elsevier Mosby 2005.