Sudden Chest pain and SOB with a Wide Complex Tachycardia

This case was contributed by a medic who wishes to remain anonymous (his comments are in red).

This was a 60 something male who called for sudden onset of severe chest pain and dyspnea. No medical history or medications. 

Upon arrival he was in extremis with altered mentation, cyanosis and diaphoresis . We were unable to get an initial ECG due to diaphoresis but the pulse ox showed a sat of 53 and a rate of 170 without palpable radial pulse. 

Initial ECG:
There is a wide complex tachycardia at a rate of 148.
What is it?
Smith Interpretation:

It is fast and the patient is in extremis, so electricity is the appropriate treatment.  If the patient were only moderately ill, you could try adenosine.

Do you think adenosine would work?

I think it would.  This has a fairly convincing LBBB pattern, with rapid depolarization of the first part of the QRS in V1-V3.  

Aside: One person commented that there is concordance in precordial leads (all QRS in the same direction without an RS-waves).  This is an excellent observation, however not quite true!  There is not really concordance: there is an rS in right precordial leads, just as in LBBB. True concordance would not have that (small) r-wave, which is best seen in V3.

However, the LBBB is not entirely convincing: look at inferior leads, which have a notch in the downstroke of the S-wave.  Thus, the depolarization is NOT as fast as it is in precordial leads, and leads one to think that this is possibly VT.  

So the differential is:
1. VT vs. 
2. SVT (flutter, AVNRT, AVRT) with LBBB and a “fragmented QRS.” 

If this is LBBB with a fragmented QRS, it is similar to, but not identical to, Chapman’s sign (notch on the ascending limb of the R-wave in I, aVL, or V6 in LBBB) or Cabrera’s sign (notch greater than 50 ms on the ascending limb of the S-wave in one of V3-V5 in LBBB).

A sudden (paroxysmal) regular tachycardia (without P-waves) that looks like LBBB is likely to be supraventricular with “aberrancy” (the “aberrant” conduction being due to LBBB).

If so, it will usually be responsive to adenosine. If not, it will be safe in VT.  So if the patient is not in extremis, adenosine is a fine alternative to electricity.

Fragmented QRS is defined as: The RSR′ pattern includes various morphologies of the QRS interval (QRS duration less than 120 ms) with or without the Q wave. It was defined by the presence of an additional R wave (R′) or notching near the nadir of the S wave, or the presence of 2 or more R′-waves (fragmentation) in 2 contiguous leads, corresponding to a major coronary artery territory. 

[Mithilesh K. Das, et al. Significance of a Fragmented QRS Complex Versus a Q-wave in Patients with  Coronary Artery Disease.  

Case continued

Combi pads we’re applied and showed a wide complex rhythm and synchronization was attemped, but the monitor repeatedly synced to the area in-between the QRS complexes (presumably due to the T wave?).  So we proceeded with unsynchronized cardioversion (same as defibrillation) at 100 J [probably should have been defib doses (200J) in hindsight]. 


This was recorded after unsynchronized cardioversion:
Notice that there are now P-waves (sinus tach at a rate of 112).
The QRS morphology is the same (LBBB).  
The fragmented QRS in inferior leads is still present.  
This QRS fragmentation is probably the result of an old inferior MI.

This proves that the tachycardia, which responded to electricity, was indeed supraventricular.  It could have been atrial flutter, but since there is no suggestion of flutter waves on that first ECG, it is probably due to AVNRT or orthodromic AVRT.
Somewhat later, the heart rate is decreasing.
No significant change
I work in a very rural area so we transport by ground for about 30-40 min to meet air transport. 

After cardioversion the patient improved but still had a wide complex rhythm at 120-150. Aspirin, Amiodarone and high flow oxygen were started. CPAP was initiated and serial 12 leads were recorded, a POC chem 3 showed normal K, Na and Hemoglobin.

The patient improved and was sent by air to the hospital as a STEMI alert.   He ultimately was not Cathed and spent a few days in the ICU and was discharged with a diagnosis of new onset CHF and hypertension.  After the call we were pretty sure the initial rhythm was Ventricular Tachycardia (VT), but we, as well medical control, are not sure what the ongoing rhythm was. 

We also weren’t sure about the monitor not syncing and if unsynchronized shocks we’re the best action (though I’m not sure what else we could have done without being able to change leads)?
Comment:
Excellent management.  It did not matter that the medics thought it was VT.  Electricity works fine, and when a patient is in extremis, they do not even remember the shock.

As for using automated synchronization, it occasionally is hazardous because the machine cannot find the appropriate point to synchronize, as here.  Thus, it was appropriate to change to defibrillation in this case.

Beware Automated Synchronization for Cardioversion!

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Comment by KEN GRAUER, MD (8/5/2018):
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Excellent discussion by Dr. Smith about this illustrative case regarding a regular WCT (Wide-Complex Tachycardia) rhythm. My thought process essentially mirrors that of Dr. Smith — to which I will add the following points. For ease of discussion — I’ve put the first 2 of the 3 ECGs shown in this case together in Figure-1.
Figure-1: Initial ECG at Time = 0 — followed by the post-conversion tracing 25 minutes later (See text).
ECG #1 (@T=0, TOP tracing in Figure-1— My preference is to always begin my assessment by describing what we see in context with the clinical situation. In ECG #1 — there is a regular WCT @ ~150/minute without clear sign of sinus P waves in a patient who is hemodynamically unstable. As per Dr. Smith, since this patient is unstable — it does not matter what the tachycardia rhythm is since regardless, immediate “electricity” is indicated. If “synch” isn’t possible — unsynchronized shock is the intervention of choice.
  • Even though electricity is immediately indicated — it is worthwhile to contemplate the Differential Diagnosis of a Regular WCT without clear sign of sinus P waves: iAlways think VT until proven otherwise (since studies show >80% of all regular WCTs without clear sign of sinus P waves turn out to be VT — andVT is the “worst” thing this could be); iiSVT with preexisting BBB (Bundle Branch Block or IVCD); iiiSVT with Aberrant Conduction; or, ivA “WPW-related” SVT.
  • Since >80% of WCTs without sinus P waves turn out to be VT — our thinking should be that we must prove the rhythm is not VT, rather than the other way around. That said, if your patient is stable — then even if you believe the rhythm is VT, this does not mean that you need to immediate cardiovert. Sometimes, medication may be tried first. That was not the case here — since this patient was unstable, and needed immediate electricity!
  • That said, as per Dr. Smith — ECG #1 looks like it may be supraventricular! That’s because QRS morphology does resemble LBBB-morphology — and, because the initial depolarization vector in many leads is rapid (straight initial deflection within the RED ovals in Figure-1). When the rhythm is VT, with the impulse originating from the ventricles and away from the conduction system — the initial depolarization vector tends to be much slower! NOTE: There is much artifact in ECG #1. Given the tenuous clinical condition of this unstable patient, this is totally understandable! But, it’s important to recognize that because of this artifact, ECG assessment is much more challenging.
  • Beyond-the-Core: Although QRS morphology in ECG #1 resembles a LBBB pattern — it is not quite typical for LBBB because: i) We lack a monophasic (ie, all upright) QRS complex in lateral leads I and V6; ii) There appears to be an initial Q wave in lateral lead aVL; andiii) There is marked fragmentation of the QRS complex in many leads. Because of marked LVH that is so often present in patients with LBBB — many tracings with LBBB do not show an all positive R wave until lateral chest lead V7 or V8. In addition, some patients with LBBB may intermittently develop right axis deviation in the frontal plane, thought to be due to a greater degree of “relative block” in the posterior compared to anterior hemifascicle. That said, the very narrow initial depolarizations in so many leads in ECG #1 (within the RED ovals) — plus, the very steep (straight) S wave downslope in anterior chest leads both strongly favor the likelihood of a supraventricular etiology. NOTE: As per Dr. Smith, there is NOT global negativity of the QRS in all chest leads in ECG #1 — because the QRS is not all negative in all 6 leads! (instead, a small and narrow initial r wave seems to be present in virtually each of these 6 leads!).
  • As per Dr. Smith — Adenosine would have been an excellent initial drug to try IF this patient would have been hemodynamically stable at the time ECG #1 was recorded. My preference is not to use Adenosine when I am virtually sure the rhythm is VT (even though adverse effects will usually not occur, even if the rhythm is VT) — but in view of the above morphologic characteristics, I would be ~90% comfortable that the WCT rhythm in ECG #1 was supraventricular. NOTE: This means that we cannot be 100% certain that the rhythm in ECG #1 is supraventricular from this single initial tracing alone! It’s important to realize that we often have to initiate treatment based on our “best educated guess” before we know for certain what a given rhythm is.
  • As per Dr. Smith — ECG #2 proves our suspicion of a supraventricular rhythm for ECG #1 was correct — because for the most part, QRS morphology is the same after conversion to sinus rhythm as it was during the WCT (the only exception being that the QRS complex is now clearly predominantly negative in the post-conversion tracing).
  • Semantic POINT: I would not call the reason for QRS widening in ECG #1 “aberrancy”. That’s because ECG #2 shows there was preexisting BBB! My preference is to reserve the term, “aberrant conduction” for those cases in which QRS widening occurs during the tachycardia because the faster heart rate reduces recovery time in one or more of the conduction fascicles, and therefore results in QRS widening during (but not after) the tachycardia.
  • Sinus rhythm has been restored in ECG #2 (RED arrows). Note that at least in some of the QRS complexes in lead aVL (within the BLUE rectangle) — that there is ST segment coving with slight elevation. As a result — I’d be concerned about the possibility of acute or recent OMI as the cause of the tachycardia. I’ll emphasize that other than the straight “shelf” ST segment flattening in lead V6 — that we really do not see other indication in ECG #2 of recent OMI in the post-conversion tracing — so what we see here in aVL may well turn out to be nothing. But the point to be made is that by always maintaining a high index of suspicion (until proven otherwise) — you are much less likely to miss subtle but important diagnoses.

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