Very fast regular tachycardia: 2 ECGs from the same patient. What is going on?

This was written by Magnus Nossen, from Norway, with comments and additions by Smith

A 50 something smoker with no previous medical hx contacted EMS due to acute onset chest pain. Upon EMS arrival the patient appeared acutely ill and complained of chest pain. An ECG was recorded immediately and is shown below. How do you interpret the ECG?

ECG#1

There is a regular tachycardia with a ventricular rate of about 180 bpm. 

Smith comment: When there is a regular wide complex tachycardia, first assess whether it is sinus or not.  At a rate of 180, this is unlikely.  The patient is unstable.  Therefore, the first step is to cardiovert.  This can be done with adenosine or electricity.  After cardioversion, if successful, you can take a few moments to assess the 12-lead in more detail and assess the post conversion ECG.  In this analysis, it is critical to assess whether the initial depolarization is rapid or slow.  If rapid, that means that the depolarization is rapidly advancing and that it must be using conducting fibers (Purkinje fibers), and is therefore supraventricular.  Is it sinus or is it a supraventricular dysrhythmia?  Other important considerations are 1) whether is looks like a typical RBBB, LBBB, 2) whether it looks "bizarre" (meaning there are no RS complexes and, if not, whether the unipolar complexes are "concordant' (all with the same precordial polarity), and 3) whether there is a "northwest" axis (between -90 and 180).  Analysis: In V1, there is an RS and it is rapid, just over 40 ms from the onset of the r-wave to the nadir of the s-wave.  This means it is supraventricular.  It is not VT.  

Magnus explains more here:

In the limb leads there is leftward axis consistent with LAFB. What appears to be very wide QRS complexes is in fact huge ST-segment deviations. This will become more apparent if you zoom in on lead V1 or lead aVL were the J point is most easily identified. Then imagine drawing a vertical line intersecting the other QRS complexes. The ST elevation in V2-V6 as well as in I and aVL becomes easily recognizable. There are retrograde P waves visible in the ST segment of the inferior leads, most easily seen in lead II. Thus the above ECG shows a supraventricular tachycardia with retrograde P waves visible in the ST segment in the inferior leads and massive current of injury in the anterior and lateral leads consistent with extensive OMI.  Put shortly is SVT with "Shark Fin STE" and not ventricular tachycardia.

Is there OMI?  How did the PM Cardio Queen of Hearts perform: OMI with low confidence.

Within a moment of recording the first ECG the patient had loss of consciousness and the ECG on the monitor changed. 

ECG#2

What do you think?

Smith: The rate is faster.  There is no longer an RS in V1. There is now concordance.  Not only that, but the time from QRS onset to peak is now nearly 120 ms, which tells us that this is VT.

Magnus: The ECG now shows a wide complex tachycardia with a ventricular rate of about 210 bpm, which is  faster than on the initial ECG. There is definite change in the morphology of the waveforms and there is also significant change in the polarity of the QRS complexes in the precordial leads. In ECG #1 there was monophasic R-waves V2-V6. In ECG#2 there is no longer concordance of QRS complexes V2-V6. There is a gradual shift of polarity occurring throughout the precordial leads. There also is slight QRS morphologic variation during the recording making the ECG recording consistent with that of a pleomorphic VT. Resuscitation efforts were undertaken. The patient went in and out of ROSC.

The ECG below (recorded during brief ROSC) shows both normal ventricular activation (in the beginning of the recording there is sinus rhythm) and polymorphic ventricular tachycardia (second half of the tracing) In other words the ECG below proves that the first ECG does show some type of supraventricular tachycardia based on QRS morphology and QRS axis.

Is there OMI?  How did the PM Cardio Queen of Hearts perform: Not OMI with low confidence.

ECG#3

Resuscitation efforts were ongoing. ROSC was achieved shortly before new episodes of ventricular tachycardia. After amiodarone and several defibrillations and about 20 minutes after initial arrest, stable ROSC was achieved. The patient was air lifted to PCI center. The following two ECGs were recorded during transport

Is there OMI?  How did the PM Cardio Queen of Hearts perform: OMI with low confidence.

ECG#4

The ECG above and below both were recorded after ROSC was achieved. Both of the ECG essentially show the same thing. An electrocardiographically huge OMI with Shark Fin ST-elevations. The above ECG has ventricular bigeminy with RBBB and LAFB morphology. The ECG below show a very clean and text book example of triangular QRST waveform also know "Shark Fin". Added on the right is the J-point marked with vertical red line.

Is there OMI?  How did the PM Cardio Queen of Hearts perform: OMI with high confidence.

ECG#5

There was acute 100% occlusion of the proximal LAD. 

Other coronaries were normal. The hospital stay was complicated by aspiration pneumonia, recurring ventricular tachycardia and a mural thrombus. Echocardiography showed and anterior and apical WMA with estimated LVEF 40%. An ICD was placed. Troponin T peaked at "only" just above 2000 ng/L. The patient ultimately did well. 

Is there OMI?  How did the PM Cardio Queen of Hearts perform: OMI with high confidence.

Learning points from Smith:

1. Sinus tachycardia, or other SVT, with aberrancy or bundle branch block can mimic VT.

2. Sinus tach, or other SVT, with Shark Fin can also mimic VT

3. If the first part of the QRS is fast, the rhythm is likely suparventricular (including sinus)

4. If the rate is 180 or greater, it is probably not sinus.

5. If the patient is unstable, and there is a regular tachycardia, whether narrow or wide, immediate cardioversion with either adenosine or electricity is indicated.

Bonus:  What is this here?

http://hqmeded-ecg.blogspot.com/2010/11/wide-complex-tachycardia-its-really.html

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MY Comment, by KEN GRAUER, MD (9/27/2023):

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Fascinating series of tracings by Dr. Nossen — that illustrate dramatic shark fin morphology from acute LAD OMI. The patient required resuscitation for recurrent polymorphic VT — but fortunately was successfully transferred to the PCI center, where reperfusion was achieved.

Of academic interest — are the arrhythmias that developed. I focus my comment on problem-solving distinction between supraventricular vs ventricular rhythms.

• To facilitate visualization — I have consolidated in Figure-1 today's 5 tracings into 5 2-lead rhythm strips, labeled sequentially from the 5 ECGs in today's case.

Figure-1: To facilitate visualization (and to consolidate today's case) — I look at leads I and II, taken from each of the 5 ECGs in today's case.

What is the SupraVentricular Rhythm?

As I emphasize above — my discussion regarding rhythm problem-solving is academic, in that fast rhythms associated with hemodynamic instability in today's case needed electricity, without need to specify all details of the rhythm. This was the case in ECG #2 — in which this monomorphic, extremely wide and fast VT rhythm was associated with loss of consciousness.

• The patient was shocked — and then began a long intensive process of resuscitation.
• Some time after electrically converting the VT rhythm in ECG #2 — the rhythm shown in ECG #3 was recorded, in which RED arrows highlight sinus P waves for the first 4 beats in this tracing (before the rhythm deteriorated to PolyMorphic VT for the remainder of the tracing).
• 
  
• Although I initially was uncertain about the etiology of the rhythm in ECG #1 — the finding of a virtually identical QRS morphology for the 4 sinus-conducted beats that are clearly seen at the beginning of the lead II rhythm strip in ECG #3 — strongly suggested that the rhythm in ECG #1 was supraventricular! Shark fin ST elevation (well seen in lead I of ECG #1) gave the false appearance of QRS widening. This meant that the negative deflections seen just after the QRS in lead II of ECG #1 had to represent retrograde P waves with a fairly long RP' interval. Thus, retrospectively— the rhythm for ECG #1 (at least for beats #5-thru-16 in ECG #1) had to represent a reentry SVT at ~170-180/minute, with retrograde P waves.
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• VT recurred a number of times — and IV Amiodarone was given. At some point during this process, ECG #4 was obtained. Once again — knowledge of what sinus-conducted QRS complexes look like (made evident by the first 4 beats in ECG #3) — facilitated my being able to walk out regular sinus P waves (RED arrows) throughout the entire lead II rhythm strip in ECG #4. As it can be seen that the QRS complex of each even-numbered beat is wider, and has a PR interval too short to conduct — the rhythm in ECG #4 has to represent ventricular bigeminy.
• 
  
• Finally — normal sinus rhythm was achieved and maintained in ECG #5. Note that the shark fin ST elevation persists in lead I of ECG #5 — and the QRS complex of the sinus-conducted beats in this tracing can clearly be seen in lead II to be narrow.

The Arrhythmia Lesson to be Learned:

I was not initially confident about my interpretation of the rhythm in today's 5 tracings. Sometimes — a "tincture of time" with access to additional tracings is needed to "put together" the pieces of the arrhythmia puzzle.

• In today's case — Seeing those 4 sinus-conducted beats at the beginning of ECG #3 — confirmed to me that the rhythm in ECG #1 was a reentry SVT with retrograde P waves — and that the rhythm in ECG #4 was ventricular bigeminy.