ECG of the Week – 6th October 2014 – Interpretation

These ECG's are from a 55 yr old female who presented with an hour of chest pain. She was a smoker and on treatment for hypercholesterolaemia.
Check out the comments on our original post here.






ECG 1
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ECG 2
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ECG 3
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ECG 4
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I'm going to tackle the interpretation of all the ECG's in one go to save duplicating the non-essential points.

Rate:
  • 72
Rhythm:
  • Sinus rhythm
    • ECG 1 shows a sinus arrhythmia
    • ECG's 2 show regular sinus rhythm

Axis:
  • Normal
Intervals:
  • PR - Normal (~160ms)
  • QRS - Normal (80-100ms)
  • QT - 320-360ms
Segments:

  • The is progressive ST segment changes during the 4 serial ECG recordings.
    • In ECG 1 ST elevation occurs in leads aVR(1mm), V1-2(1mm), V3(3-4mm) and V4 (1mm). 
    • During the serial ECG's we see the ST elevation in leads V1-4 progress, maximal on ECG 4 with ST elevation in V1(2mm), V2(1-2mm), V3(4-5mm) and V4 (3mm).
    • ECG 3 also shows early ST elevation in the inferior leads although this is less pronounced on ECG 4.
  • ST Depression leads I, V5-6
    • As the ECG's progress the ST depression resolves in leads V5-6 (potentially prior to becoming ST elevation)

Additional:

  • Hyperacute T-waves in leads II, III, aVF, V3-6
  • T-wave in V2 progressively becomes more hyper-acute as the ECG's progress
  • Biphasic T wave V1

Interpretation:

  • Progressing antero-septal ST elevation with hyperacute T-waves
  • Likely LAD lesion, I agree with Ken that I suspected a 'wrap-around' component due to the inferior changes best seen in the 3rd ECG


What happened ?

The patient was sent for urgent coronary angiogram which showed:

  • 100% LAD occlusion --> Stented
  • 30% mid-RCA stenosis

I don't have the full angio report so can't comment on the exact location of the lesion or the anatomy of the LAD.
The patient's echo post procedure showed dital anteroseptal and anteroapical akinesis with preserved systolic function.


References / Further Reading

KG-EKG Press


Life in the Fast Lane
Dr Venkatsen's Blog



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 – 6th October 2014

These ECG's are from a 55 yr old female who presented with an hour of chest pain. She was a smoker and on treatment for hypercholesterolaemia.






ECG 1
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ECG 2
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ECG 3
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ECG 4
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The ECG's in this series were performed at 10 minute intervals.

I also want to point out that the current Australian Heart Foundation STEMI Criteria differ from those in the latest ESC and AHA guidelines. The current Australian Guidelines define a reperfusion therapy STEMI as:

  • Persistent ST elevation >1mm in 2 contiguous limb leads or
  • ST elevation >2mm in 2 contiguous chest leads or
  • New LBBB pattern

ECG of the Week – 29th September 2014 – Interpretation

This week's ECG is from a 60 yr old male who presented with 3 days of vomiting & diarrhoea.
Past medical history of hypertension and mild chronic renal impairment.
Thanks to Dr Anand Senthi for sharing this ECG case.
Check out the comments from our original post here.



Click to enlarge
Rate:

  • ~90 bpm
Rhythm:

  • Regular
  • Sinus rhythm
    • P waves best seen in the inferior leads
    • P waves difficult to see in the precordial and high-lateral leads
Axis:

  • Normal
Intervals:

  • PR - Prolonged (~240ms)
  • QRS - Prolonged (120ms)
  • QT - ms (QTc Bazette 380-400 ms)
Segments:
  • Nil significant abnormality
Additional:
  • Not typical LBBB or RBBB morphology given QRS widening
  • Peaked T waves leads V2-6
Interpretation:



  • ECG Features suggestive of hyperkalaemia


What happened ?

The patient had an urgent VBG which showed a K+ of 8.0 mmol/L ! 
Therapy with calcium gluconate, nebulised salbutamol and insulin/dextrose was commenced. 

Following treatment the ECG was repeated as is shown below:

ECG Post Treatment of Hyperkalaemia
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This ECG shows resolution of PR prolongation, QRS widening and T wave peaking seen on the first ECG.

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 – 22nd September 2014 – Interpretation

Sorry but I don't have any clinical information on this ECG at all but that hasn't stopped us before.

So what's going on here ?

Check out the great discussion on this ECG in the comments section from our original post.

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Numbered Ventricular Complexes
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Rate:
  • Mean ventricular rate 54 bpm
Rhythm:
  • Interesting !
  • P waves
    • Precede all ventricular complexes
    • P waves occur regularly every 760 ms
    • EXCEPT between complexes #2/3, 4/5, 7/8 where the P waves is dropped
    • The gap between the P waves either side of the pause is 1520 ms 
      • i.e. double the normal P-P interval
  • QRS Complexes
    • Progressive PR lengthening
    • Progressive R-R shortening
    • Grouped beatings
    • The dropped QRS is not preceded by a P wave
      • Not just 2nd Degree AV Wenckebach
Axis:
  • Normal
Intervals:
  • PR - Initially normal (180ms) then progressive lengthening
  • QRS - Normal (100ms)
  • QT - 440ms 
Segments:

  • ST Depression leads II, III, aVF, V2-6

Additional:

  • T wave inversion Leads III, aVR, V1-3
  • rSR' Pattern V1
  • Deep inferior Q waves with smaller lateral Q waves
  • Baseline irregularity
  • Lead I rhythm strip makes P waves more difficult to identify

Interpretation

So we have clear evidence of a AV Wenckebach but where do the P waves go ?

Frequent ECG of the Week commenter / ECG author / blogger / legend Ken Grauer shares his thoughts on our missing P waves:

I strongly suspect that there is a blocked PAC that causes the pause (and terminates the Wenckebach cycles) - but unfortunately in the long lead I it is very difficult to be certain of this ... I do think I see tiny-but-real differences in the T wave of the beats that initiate the pause (in lead II for beat #2; in aVF for beat #4; and in V2 for beat #7)

My other theory:

Presence of a 2nd Degree Type II SA exit block in addition to our 2nd Degree Type I AV block !
There is a regular P-P interval with the interval including the dropped P wave being twice that of the normal P-P interval. The causative factors for both types of block are virtually identical - ischaemia, drugs, electrolyte abnormality, cardiomyopathy, myocarditis etc.

Do I have a definitive answer ? No

I don't have any other ECG's or clinical information on this case. A longer rhythm strip, serial ECG's, old ECG's, more clinical information, and ideally lead II as the rhythm strip may shed more light on the likely rhythm disturbance and causative factors.

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.