ECG of the Week – 28th November 2016

The following ECG's are from a 62 yr old female who presented with chest and epigastric pain. The first ECG was performed by the patient's GP and the second ECG on arrival in the Emergency Department. Her pain was ongoing at the time of both ECG's and she has a past medical history of hypertension, obesity and T2DM.




ECG from GP
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ECG on arrival ED
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Things to think about

  • What are the key ECG features in each ECG ?


ECG of the Week – 21st November 2016 – Interpretation

This ECG is from an 89 yr old female who presented with abdominal pain and fever. She has a PPM in-situ and a history of ischaemic cardiac disease.




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Rate:
  • 72 bpm
Rhythm:
  • Intrinsic atrial activity
  • Ventricular paced rhythm
    • Complexes #1-10, #12 
    • All preceded by v-pacing spike - see below for more information
  • Sinus / native ventricular complex
    • Complex #11
Axis:
  • Left Axis Deviation
Intervals paced complexes (#1-10, #12)
  • PR - Variable (160-200ms)
  • QRS - Variably prolonged (100-160ms)
Intervals sinus complex (#11)
  • PR - Normal (140ms)
  • QRS - Normal (100ms)
Additional:
  • Variable QRS morphology of paced complexes
    • Complexes #1-4,6,9,12 all have similar morphology
    • Complexes #5,7,8 preceded by pacing spike but morphology similar to native complex (#11) best appreciated in rhythm strip
  • ST Depression and deep T wave inversion in native QRS complex #11
  • Morphology of QRS in leads V1-2 not typical for LBBB with Rsr' in v2

Key features of interest:
  • Lack of typical LBBB pattern in leads V1-2 with RSR pattern in lead V2
    • This can be seen in cases of pacing lead malposition or migration but can also be seen in appropriate RV pacing - see below for a detailed explaination
  • Deep T wave inversion in the native (non-paced) QRS complex seen in the lateral leads
  • Variable QRS morphology of the paced complexes
    • Due to variable fusion of native and paced QRS complexes

Is RBBB morphology during right ventricular pacing always due to pacing 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.

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 between 0 and -90 degrees and;
  • Precordial transition point before lead V3
And / or:
  • Repositioning of leads V1-2 one interspace lower with resolution of RBBB features
In this ECG the frontal plane axis is between 0 and -90 deg with a precordial transition from positive to negative QRS between leads V2-3. These features support correct RV lead placement rather than lead migration and may be seen with inappropriate ECG lead positioning.

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

What about the native QRS in leads V4-6

The broad differentials for the changes on the native complex 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 the non-paced complex 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. 
The following 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.

Pseudo-fusion

Complexes #5,7,8 are all proceeded by a pacing spike but have a QRS morphology similar to native sinus complex. This is due to pseudo-fusion which occurs when the pacing rate and native sinus rate are close together. This is a benign condition but does result in unnecessary pacemaker activity. 

We have another example of pseudo-fusion here:
You can find a nice overview of pseudo-fusion and fusion beats in paced rhythms here:


References / Further Reading

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 – 14th November 2016 – Interpretation

The following ECG's are from an 84yr old male who presented following an episode of syncope in which he sustained a head injury. 
The initial ECG was taken on presentation to the Emergency Department and the second ECG was performed several hours later. The patient was asymptomatic on both occasions with a normal blood pressure. 

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Initial ECG on presentation
Key features:
  • Bradycardia - mean ventricular rate 54 bpm
  • Marked sinus arrhythmia
    • ~2 sec pause between 1st and 2nd complex
  • Inferior axis
  • 1st Degree AV block - varying magnitude 220-280 ms
  • Right bundle branch block
  • Discordant ST / T wave changes
    • ST Elevation leads aVR, aVL
    • ST Depression leads II, III, aVF, V6 with T wave inversion

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ECG several hours later
Key features:

  • Bradycardia - mean ventricular rate 36 bpm
  • Marked sinus arrhythmia
  • Morphology of axis, QRS, ST segments and T waves same as prior ECG

Interpretation:
  • Sinus Node Dysfunction
    • Marked sinus bradycardia
    • History of collapse / syncope
 The following AFP article has a nice general overview of sinus node dysfunction / sick sinus syndrome:

What happened ?

The patient remained asymptomatic during episodes of bradycardia. There were no correctable electrolyte abnormalities or culprit medications to account for bradycardia.<35 a="" an="" and="" bpm="" bradycardia="" cardiac="" chamber="" diagnosis="" dual="" during="" dysfunction="" font="" given="" his="" history="" hospitalization.="" insertion.="" made="" marked="" node="" noted="" of="" on="" pacemaker="" patient="" sinus="" syncope="" telemetry="" the="" underwent="" uneventful="" was="">
A diagnosis of sinus node dysfunction was made and a dual chamber pacemaker was inserted. The patient made an uneventful post-procedural recovery and was discharged home following a brief in-patient stay.

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 – 14th November 2016

The following ECG's are from an 84 yr old male who presented following an episode of syncope in which he sustained a head injury. 
The initial ECG was taken on presentation to the Emergency Department and the second ECG was performed several hours later. The patient was asymptomatic on both occasions with a normal blood pressure. 



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Initial ECG on presentation

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ECG several hours later


Things to think about

  • What are the key ECG features ?
  • What are your differentials for these features ?
  • What other considerations are there in his management / investigation ?