ECG of the Week – 22nd August 2016 – Interpretation

This ECG is from a 20 yr old female who presented following an episode of palpitations with associated chest pain and dysponea.



Click to enlarge

Rate:

  • 60

Rhythm:

  • Sinus arrhythmia

Axis:

  • Normal

Intervals:

  • PR – Short (~100ms)
  • QRS – Prolonged (120-130ms)
  • QT – 440ms (QTc Bazette 440 ms)

Segments:

  • ST elevation leads III, aVF <1mm with flat morphology

Additional:

  • Delta waves leads I, V1-4
  • Pseudo right ventricular hypertrophy secondary to pre-excitation rather than actual chamber enlargement with the following ECG features:
    • Dominant R wave leads V1-6
    • R/S ratio >1 in lead V1
    • T wave inversion leads aVL, V1-3

Interpretation:

  • Wolff-Parkinson-White Syndrome
    • Left posterior / left posterolateral accessory pathway using Arruda algorithm

What happened ?

The patient had known pre-excitation and had been non-compliant with beta-blocker and sodium-channel blocker therapy. The patient was admitted for telemetry and re-instigation of anti-arrhythmic agents prior to ablation consideration / planning.

References / Further Reading

Life in the Fast Lane

Textbook

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

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.


Click to enlarge

Rate:

  • 72 bpm

Rhythm:

  • Regular

Axis:

  • Normal

Intervals:

  • PR – Normal (140ms)
  • QRS – Normal (100ms)

Segments:

  • 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

Additional:

  • P waves difficult to see due to baseline artifact – best seen in V2-3
  • T wave inversion leads aVR, aVL, V1-2

Interpretation:

  • 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 www.brugadadrugs.org 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

Textbook

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