My thanks to Sophie Markwick from England for her permission to use these 12 leads for educational purposes.
 
 
This patient called emergency services for chest pain and vomiting. He takes no medications and has no known medical history. The chest pain started at 5pm, he did not call 911 until almost 2am when the pain increased and he began vomiting. He was found A&O yet grey in color. While obtaining the initial 12 lead, he complains of feeling hot and collapses.
Normally, I would show you the full tracing first, however, with this case, I have decided to show the Hexaxial leads first – Fig. 1 – I think the full tracing will draw the readers eye away from these leads which could potentially cause you to miss some important findings:

*Although the tracings captured are not flat, I believe we can still reliably interpret these 12 leads.

Fig. 1

 

 

 

Fig. 2

Red boxes = Contiguous “High Lateral” Leads /  Green boxes = Contiguous Inferior Leads

 

  • We have a Sinus Rhythm at ~75 bpm. We can say this is Sinus because the P waves in Lead II are upright and negative in AVR.
  • There is a bit of artifact on the baseline, We can say this is not A Fib due to the R-R being regular. The PR Interval falls into normal limits.
  • The Q waves in AVL appear right at 40ms wide and although the depth is not even close to 1/3 – 1/4 the height of the QRS, they are still, suspicious for being pathologic.
  • The QRS are narrow at ~94ms
  • ST Deviations: (J point relative to the PQ Junction) All 3 inferior Leads have significant ST depression of about 2-4 mm depending on the complex and lead.
  • The “mirror image” opposite of Lead III is AVL which shows ~2-3 mm of STE. In addition, it’s contiguous lead I also shows minimal but present STE indicative of occlusion.
  • The Axis is shifted severely left noted by the predominantly negative QRS in AVF.
General Comments:
              -The overall voltage of the QRS complexes are a bit larger than expected – this could indicate an underlying hypertrophied ventricle.
          IF hypertrophy is present: This could alter the presentation of “normal” depolarization meaning LVH can produce a “STEMI Mimic” giving us a false positive. 
              -In addition – Lead III has a convex down – down sloping ST segment appearing as a “Strain” pattern – another convincing argument for LVH. 
             -Although the ECG has low specificity for atrial enlargement, a few of the P waves do appear somewhat flattened and possibly minor notching (LAA). Echo would be needed to confirm or rule out chamber enlargement.
 
 
Now for the full tracing:

 

Fig. 3

 

 

As you can see, the computer interpretation got some of it right but didn’t know to what to make of the sudden transition in the rhythm. In my experience, most people would call this a transition to Torsades, however, I would have to disagree.
  • Torsades de Pointes is a variant of Polymorphic VT associated with a Long QT Interval – not seen here. In most cases, we would need a previous ECG to compare the QT OR we would have to quickly inspect the underlying QT post electrical therapy. Here, we have it readily available all in 1 tracing.
*In most cases, synchronized cardioversion will be impossible due to the irregularity of the QRS. Defibrillation is more often indicated.
*Polymorphic VT without prolonged QT is most likely from an ischemic nature.
 
Causes of a prolonged QT are numerous including, but not limited to:
  • Genetic mutation causing Congenital Long QT Syndrome
  • CNS catastrophe
  • Metabolic Derangements
  • Medication induced

Crediblemeds.org keeps an updated list of medications that prolong the QT. It’s free, however it does require registration:

https://www.crediblemeds.org/healthcare-providers

                       *NoteI have no affiliation with this website and I do not gain any monetary value by promoting it.
 
♦ Polymorphic VT with Long QT responds well to Magnesium whereas drugs such as Amiodarone and/or BB work better with a Short QT.
 
           Back to the case – So what happened??
 
We have a Sinus Rhythm that suddenly changed into an Irregular Wide Complex Tachycardia. This certainly is not typical VT noted by the severe degree of irregularity in the QRS morphologies and we can see a “twisting of the points” best seen in the right precordials – this is the QRS Axis “swinging” from positive to negative.
– V6 gives an almost coarse V Fib appearance.
        *Many times, what is thought to be “Torsades” is actually VF*
Here, I believe this has a very organized appearance indicating Polymorphic VT and not VF. Granted, if there is no quick intervention – this probably will deteriorate into VF.
In Fig. 4, I have enlarged and marked the tracing in AVL to show both the Absolute Refractory Period (where if an impulse were to fall into this, no response from the myocardium would take place) and the Relative Refractory Period noted by the peak of the T wave.
I measured (an arbitrary point) from the onset of the Q to the peak of the T wave – labeled with the red “H” marks; I used the first complex in AVL then “copied and pasted” measuring the 2nd complex – it is identical. Then the 3rd. Here you can now see the following impulse “landed” just after the peak of the T wave into the Relative Refractory Period causing the “R on T” Phenomenon setting in motion the Polymorphic VT with underlying short QT.

Fig. 4

 

The providers on scene lowered the patient to the floor, confirmed he was pulseless and initiated CPR. Defibrillation delivered without response, CPR continued for 2 minutes and a second defibrillation delivered. ROSC was then achieved and the patient regained consciousness.
 
Here is the post ROSC tracing 17 minutes after the initial 12 lead en route to the PCI capable hospital:

Fig. 5

We are now back to Sinus. The hexaxial leads look nearly identical to the 1st tracing with STE in AVl (minimal if any STE in I) and reciprocal STD in the Inferior leads. We now we have a good look at the precordial leads.
 
  • There is significant ST Elevation from V1- V3 with maximal STE in V2 which appears to be ~9 mm, severely out of proportion to the QRS even if LVH were present.
  • All 3 of these leads also show a Q wave
  • Not that it is needed to confirm occlusion here, but V3 also happens to present with “Terminal QRS Distortion” where there is no S Wave and no J Point Notching – indicating an occlusion of the LAD.
  • V4-V6 shows notching on the downstroke of the R wave. I would label this QRS Fragmentation – indicative of new or old “scarring” in the myocardium.                                                                                                                                        *This scarring of the tissue does not conduct, therefore the impulse must “zig zag” around it creating this extra       notching.
  • V4 clearly has a hyperacute T wave
  • V5/V6 shows ST depression

See Fig. 6 for details:

Fig. 6

 

 In Fig. 7, note the time stamp at 03:02 – 33 minutes following the previous tracing.

  • We now have clear STE in both leads I and AVL
  • Again, reciprocal STD in all 3 Inferior Leads
  • The ST Segment in V1 has straightened out
  • The STE in both V2 -V4 has grown
  • The STD in V5 has actually improved with the STD in V6 about the same.

 

Fig. 7

 

  • The pt was found to have a large occlusion in the LAD, was stented with good outcome.                                           *So if there were clear ST elevation in AVL in the presenting ECG and in Lead I in the follow up, why was there no occlusion found in the LCX? – The reciprocal of the Anterior leads are the Inferior leads. The reciprocal of the Inferior are the Lateral and so on. See Fig. 8 below for all reciprocal leads.
In the case here, I believe the extensive ST elevation in the V1-V3 showed reciprocal ST depression in the Inferior leads thereby showing its reciprocal STE in leads I and AVL.

Fig. 8

P = Posterior
A = Anterior
I = Inferior
L = Lateral                                                               “Don’t forget your PAILS”

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