EXTRA COPY — ECG Blog #536 — Why 2 Morphologies? — EXTRA COPY

The ECG in Figure-1 was sent to me for my thoughts. Initially I had no clinical information.

QUESTIONS:

• What is the rhythm?  
• Why are there 2 different QRS morphologies?
• What is the likely underlying cause of this rhythm?

Figure-1: The initial ECG in today's case — initially sent to me without clinical information. (To improve visualization — I've digitized the original ECG using PMcardio).

My Thoughts:

The overall rhythm in Figure-1 appears to be regular with obvious QRS widening — and a ventricular rate of just under 100/minute (ie, with an R-R interval just over 3 large boxes in duration).

• There are 2 different QRS morphologies.
• Although the R-R interval varies slightly — I attributed this to uncertainty regarding where the QRS begins in some leads.
• P waves are absent. The only suggestion of atrial activity that I saw is possible retrograde P waves in some chest leads.

PEARL #1: This tracing emphasizes the important concept that, "12 leads are Better than One" — because if you only looked at leads I and V1 (and/or at leads V2,V3,V4) — it would be easy to think the rhythm was simply AIVR (Accelerated IdioVentricular Rhythm). 

• Instead, as shown in Figure-2 — there clearly is an alternating QRS morphology that is seen every-other-beat.

Figure-2: For clarity — I've numbered the beats in the limb leads. 

What is Going On?

Based on what I saw in Figure-2 — I thought the following:

• There is a regular wide QRS rhythm at ~95/minute — but without clear sign of atrial activity. QRS morphology is not consistent with any known form of conduction block — so this most likelly represents a ventricular rhythm.
• Many leads strongly suggest that QRS morphology alternates every-other beat — but without explanation as to why this may be so (ie, There are no P waves that may be conducting — and no significant variation in R-R intervals that might be producing a rate-related effect).
• BOTTOM Line: I was left with the conclusion that the rhythm in Figure-2 most likely represents the rare arrhythmia known as BiDirectional VT.

Semantics:

I've previously reviewed the concept of "AIVR" (Accelerated IdioVentricular Rhythm) — which is a slower form of "VT" (See ECG Blog #108).

• Technically, AIVR is not "VT" — because the ventricular rate is not ≥100/minute. But the ventricular rhythm known as AIVR clearly is faster than the usual ventricular "escape" rate, which normally is between 20-40/minute ==> the designation preferred by many is that AIVR represents a form of "slow VT".
• As emphasized in Blog #108 — the importance of recognizing AIVR depends on the clinical setting in which it occurs (ie, AIVR often occurs as a reperfusion arrhythmia in patients who have had a recent MI).
• PEARL #2: Whenever I see AIVR — I carefully consider the possibility that the patient may have had a recent MI that could have passed undetected.

What is BiDirectional VT?

I presented a case of bidirectional VT in ECG Blog #436:

• As discussed in ECG Blog #231 — bidirectional VT is a special form of VT, in which there is beat-to-beat alternation of the QRS axis. This unique and very uncommon form of VT is distinguished from PMVT (PolyMorphic VT) and from pleomorphic VT — because a consistent pattern of alternating QRS morphology is seen every-other-beat throughout the VT episode.
• Typically with bidirectional VT — there are alternating longer-then-shorter R-R intervals that correspond to the alternating QRS morphology. That said — as was seen with the case I presented in ECG Blog #436 (as well as with today's case) — QRS widening with uncertainty in some leads as to where the onset of the QRS begins may render it difficult to distinguish subtle alternation in R-R interval duration from what otherwise appears to be a fairly regular ventricular rhythm.
• Technically — this raises the question as to whether today's rhythm might simply represent AIVR with alternating exit sites accounting for the alternating QRS morphology (as I allude to in my discussion of ECG Blog #231). While fully acknowledging these theoretical considerations — My impression of today's rhythm remains unchanged = the most likely explanation for the rhythm in Figure-1 is bidirectional VT.

PEARL #3: There are a limited number of causes of bidirectional VT. As reviewed by Almarzuqi et al (Vasc Health Risk Mgmt 18:397-406, 2022) — Potential Causes of Bidirectional VT include:

• Digitalis toxicity.
• CPVT (Catecholaminergic PolyMorphic VT).
• Acute myocardial ischemia.
• Familial hypokalemic periodic paralysis.
• Cardiac Sarcoidosis.
• Primary Cardiac Tumors and/or Cardiac Metastasis.
• Andersen-Tawil Syndrome ( = Long QT Syndrome, Type 7).
• Acute Myocarditis.
• Certain drug overdoses (Aconitine poisoning, severe caffeine poisoning).

PEARL #4: Given how rare bidirectional VT is — the 1st thing to do when contemplating this diagnosis is to consider whether the patient might have one of the above-listed potential causes of this rhythm.

• In years past — Digitalis toxicity used to be the most common cause of bidirectional VT. This no longer appears to be true — given the overall reduced use of Digoxin (and in those cases in which Digoxin is still prescribed — toxicity is much less common nowadays because dosing of this drug is so much less than it used to be). 
• With the exception of myocardial ischemia and myocarditis — the other entities listed as potential causes of bidirectional VT are rare (which explains why bidirectional VT is rare).
• To Emphasize: In my experience — bidirectional VT is not a common manifestation of myocardial ischemia. But the PEARL is that ischemia/infarction should always be considered whenever you contemplate a diagnosis of bidirectional VT.
• Clinically: The BEST treatment of bidirectional VT — is to identify the causative condition in the hope that there may be effective treatment of that condition.

Follow-Up in Today's CASE:

It turns out that today's patient was a previously healthy middle-aged woman — who presented to the ED (Emergency Department) with new-onset CP (Chest Pain). The patient's condition rapidly deteriorated with resultant cardiac arrest.

• A complicated course followed, fortunately with successful ROSC (Return Of Spontaneous Circulation) — and, at the earliest opportunity cardiac catheterization was performed.

QUESTION:

• What do you think cardiac cath showed?  

HINT #1: To facilitate assessment of QRST morphology for the 2 "families" of QRS complexes — in Figure-3, I've enclosed beat #3 and beat #6 within the BLUE and RED dotted rectangles. 

Figure-3: To facilitate assessment of QRST morphology — I've enclosed beats #3 and #6 within BLUE and RED dotted rectangles.

HINT #2: To facilitate concentration on ST-T wave morphology even more for the 2 "families" of QRS complexes — I've shaded out the remaining beats in the limb leads.

Figure-4: I've shaded out the remaining limb lead beats.

Answer:

Today's rhythm is bidirectional VT. This means that there are no normally conducted QRS complexes — but instead, all beats on today's tracing are ventricular in etiology.

• PEARL #5: Most acute OMI (Occlusion-based MI) tracings identified by ECG will be diagnosed on the basis of ST-T wave morphology changes in sinus-conducted beats. Assessment of ST-T wave morphology in PVCs is usually not a reliable indicator of an acute event.
• That said — On occasion, the shape of ST-T wave elevation or depression in one or more PVCs may be diagnostic of acute infarction. This is precisely what we for the PVCs in ECG Blog #359.
• NOTE: For an example of a case in which assessment of the normal (sinus-conducted) beats was not definitive for acute OMI — such that the diagnosis of acute infarction was only made by recognizing the abnormal ST-T wave morphology of several PVCs — See My Comment at the bottom of the October 8, 2018 post in Dr. Smith's ECG Blog.

Applying the advanced concept from PEARL #5 to today's tracing — the shape of ST-T wave morphology in Figure-5 is clearly disproportionate and "off" from what we'd expect for both QRS families. Specifically:

• The QRS family of odd beats in Figure-5 (illustrated by beat #3) — shows inappropriate ST elevation in the inferior leads with reciprocal ST depression in lead aVL (the RED and BLUE arrows in these leads).
• More subtle, but still evident — the QRS family of even beats (illustrated by beat #6) — shows inappropriate ST elevation in each of the inferior leads (which is especially apparent in lead II given tiny size of the QRS in this lead).
• Both families of QRS complexes show a disproportionately increased amount of ST depression in the mid-chest leads of Figure-5 — with the BLUE arrows in leads V2,V3,V4,V5 of the even-numbered beats highlighting the obvious abnormality of this finding by the marked amount of horizontal (ledge-like) ST depression.

CASE Conclusion: 

Today's ECG illustrates a case of bidirectional VT that developed as a result of acute infero-postero OMI. This was confirmed on cardiac catheterization that showed multi-vessel disease with acute total occlusion of the LCx (Left Circumflex) coronary artery.

Figure-5: Both families of QRS complexes suggest that the cause of this bidirectional VT is acute infero-postero OMI. 

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Acknowledgment: My appreciation to Fardeen Baray and Hameedullah Ahmadzai (from Kabul, Afghanistan) for the case and these tracings.

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