ECG Blog #538 — An Unusual Finding

The ECG in Figure-1 was obtained from an adult who complained of frequent “palpitations”.  Imagine no history is available.

Choose the BEST Answer regarding the rhythm in Figure-1:

• a) The probability of VT is ~50%.
• b) The probability of VT is ~75%.
• c) The probability of VT is virtually 100%.
• d) The rhythm is a reentry SVT (ie, AVNRT or AVRT) with aberrant conduction.
• e) The rhythm is AFlutter with 2:1 AV conduction. 

Figure-1: The initial ECG in today's case — obtained from an adult with frequent "palpitations". (To improve visualization — I've digitized the original ECG using PMcardio).

My Initial Thoughts:

The rhythm in Figure-1 is a regular WCT (Wide-Complex Tachycardia) at ~160/minute, without clear sign of sinus P waves.

• As always, the diagnosis of VT must be considered until you prove otherwise — whenever you encounter a regular WCT rhythm without clear sign of sinus P waves.

Additional factors in favor of VT include the following:

• The frontal plane axis during the WCT rhythm is indeterminate (predominantly, but not completely negative in both leads I and aVF). This degree of frontal axis deviation favors VT — because it is not consistent with either LAHB (Left Anterior HemiBlock) or LPHB (Left Posterior HemiBlock) conduction. That said, because the frontal plane axis is not “extreme” (ie, not completely negative in either lead I or aVF) — this degree of axis deviation is suggestive but not diagnostic of VT (See Rule #1 and Table-2 in ECG Blog #42-bis, among many other examples throughout my ECG Blog of "extreme" axis deviation as a sign of VT).
• QRS morphology in lead V1 is all positive, but amorphous (ie, completely lacking in the triphasic rsR’ morphology characteristic of RBBB conduction). Although this lead V1 appearance does not completely rule out RBBB conduction (from either preexisting bundle branch block or rate-related aberrant conduction) — this QRS morphology does somewhat favor VT (as per Figure-2 in ECG Blog #42-bis). That said, wide terminal S waves are seen in left-sided leads I and V6 — and there is enough of a positive r wave in lead V6 such that RBBB conduction is still possible (ie, QRS morphology in Figure-1 is suggestive but not diagnostic of VT).
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• BOTTOM Line: At this point in our assessment — We lack a definitive answer. Without knowledge of this patient’s age, awareness of his/her prior medical history (ie, Any history of underlying heart disease?) — and without the benefit of a prior ECG that might reveal similar QRS widening during sinus rhythm — We are left with the statistical reality that the clear majority of regular WCT rhythms with atypical morphologic features and without clear sign of sinus P waves (as is the case in Figure-1) — are likely to be VT (although some of these regular WCT rhythms will turn out to be supraventricular).
• Looking again at the answer choices provided at the beginning of today’s post — the BEST choice would seem to be b) The probability of VT is ~75%.

BUT — There is One More Important Clue!

• HINT #1: This KEY clue that I have not yet mentioned tells us that the answer is not choice "b" — but something else. This KEY clue is related to atrial activity.

Take another LOOK at Today's Tracing in Figure-2:

• HINT #2: Why have I numbered the beats in Figure-2?

Figure-2: I've numbered the beats in today's tracing.

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Answer: The Clue provided by Atrial Activity ...

It turns out that atrial activity is present in today's tracing — in the form retrograde P waves (highlighted by YELLOW arrows in Figure-3).

Figure-3: YELLOW arrows highlight retrograde P waves.

Retrograde P Waves:

Retrograde P waves typically appear as a negative notch or a negative deflection that occurs after the QRS in one or more of the inferior leads (ie, P wave negativity in the inferior leads being an indication that atrial depolarization is moving away instead of toward the AV Node).

• PEARL #1: The finding of AV dissociation during a regular WCT rhythm is an important clue that a regular WCT rhythm is the result of VT (as was shown in ECG Blog #133). But the finding of consistent 1:1 VA (retrograde) conduction is not AV "dissociation" — because in this case, each QRS complex is related to each neighboring QRS complex (ie, by a constant RP' interval). Both VT and reentry SVT rhythms may manifest consistent 1:1 VA conduction — such that the finding of 1:1 VA conduction during a regular WCT rhythm is of no assistance for distinguishing between VT vs an SVT rhythm (See ECG Blog #240 — for full discussion of the role that consistent 1:1 retrograde atrial activity may play in sustaining the reentry SVT rhythms of AVRT and AVNRT).
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• PEARL #2: In Figure-3, we do not see consistent 1:1 VA conduction — because retrograde P waves are not seen after each QRS complex (ie, There is no retrograde P wave seen after the QRS of beats #6, 12, 18 and 21 in Figure-3).

Looking Closer at Today's Retrograde Activity ...

To better visualize the nature of retrograde atrial activity in today's tracing — I've magnified in Figure-4 an excerpt of of beats #5-thru-15 from Figure-3.

• Can you appreciate what's happening to the RP' interval following beats #7-thru-12?

Figure-4: I've magnified beats #5-thru-15 from Figure-3. What's happening to the RP' interval following beats #7-thru-12?

Laddergram Illustration:

My laddergram in Figure-5 schematically shows that the RP' interval is progressively increasing as we move from beat #7 to beat #11 (dotted RED lines after these beats) — until we see that there is no retrograde P wave after beat #12.

• Retrograde conduction resumes after the brief pause between beats #12-13 — albeit once again with a shorter retrograde RP' interval after beat #13.
• PEARL #3: With this laddergram in Figure-5 — the YELLOW arrows represent retrograde P waves. Although subtle, the RP' interval is increasing. This is most easily appreciated by looking at the RP' interval before the retrograde Wenckebach conduction is blocked (darker BLUE double arrows seen in the rhythm strip after beat #11). Note subtle increase in the AV Nodal Tier in the angle of retrograde P wave conduction, that becomes maximal just before the P wave is dropped (dotted BLUE line in the AV Nodal Tier). And then, following the brief pause between beats #12-13 — the Wenckebach cycle begins again with the RP' interval shortening after beat #13. 

Figure-5: Laddergram showing retrograde Wenckebach conduction for magnified beats #5-thru-15 from Figure-4.

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Significance of Intermittent Retrograde Conduction

In Figure-6 — I've drawn theoretical laddergrams to illustrate why the presence of intermittent retrograde conduction that does not disturb the regularity of a WCT rhythm is virtually diagnostic of VT (Roig et al — Circulation 153(15):1171-1173, 2026 — and — Pilecky et al — Eur Heart J 7:1-2, 2023).

• Panel A (Top laddergram in Figure-6) — A PAC (beat #3) is seen after 2 normal sinus beats. If the timing is "just right" — this PAC may initiate a reentry SVT rhythm (usually either AVNRT or AVRT). But because reentry SVT rhythms are dependent on continued retrograde conduction (dotted lines during the SVT run from beat #3-thru-11) — the reentry SVT will abruptly end if for any reason retrograde conduction fails (as it does here in this theoretical laddergram after beat #11).
• Panel B (Bottom laddergram in Figure-6) — Following 2 sinus beats, a run of VT begins with beat #3. I've drawn in some different possibilities for different VA conduction ratios. It should be apparent in Panel B that regardless if 1:1 VA conduction persists (as it does from beats #4-to-9) — or is intermittent with a 2:1 VA conduction ratio (as it is from beats #9-to-12) — or manifests retrograde Wenckebach conduction with progressive RP' prolongation until retrograde conduction fails (as occurs from beats #13-to-17) — the regularity of the VT rhythm is unaffected! This proves that ventricular activation is independent of atrial activity — thereby essentially confirming VT by eliminating the possibility of a reentry SVT that is dependent on persistence of retrograde conduction with a reentry circuit.

Figure-6: Theoretical laddergrams illustrating the expected effect of intermittent retrograde conduction on a reentry SVT vs the effect on VT.

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Final Thoughts on Today’s CASE:

Intermittent block of retrograde conduction during a regular WCT rhythm (be this by retrograde Wenckebach or other intermittent VA conduction phenomenon) — is not a common occurrence. This is an advanced concept that you will not often see. But it does occur (as in today's case) — and you can detect it if looked for.

• Going back to Figure-1 (and to Figure-3) — the fact that the WCT rhythm in today's case maintains a regular ventricular rate despite the failure to conduct retrograde with every beat essentially proves that this WCT rhythm is sustained VT (with the only rare exception being the possibility of a wide junctional tachycardia that conducts retrograde).

Clinically — this subtle informative clue of intermittent retrograde conduction during a regular WCT rhythm will usually not be needed to determine optimal initial management. 

• This is because IF your patient in a regular WCT rhythm without sinus P waves is hemodynamically unstable — then electrical cardioversion will be needed regardless of whether the rhythm is VT or an SVT.
• IF on the other hand, your patient in a regular WCT is stable — then a trial of medical therapy is reasonable. And, if you do recognize intermittent retrograde conduction despite maintenance of the regular WCT rhythm — then I'd skip a trial of Adenosine, because we would then know that the WCT rhythm is VT.

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Acknowledgment: My appreciation to Khaled Elashiq, Hasan Al-Qassim and Mahmoud Al-Rahmoun (from Syria) for contributing this case.

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ECG Blog #537 — What is the Rhythm?

The ECG in Figure-1 was obtained from an older woman with diabetes — who presented with acute dyspnea.

QUESTIONS:

• What is the rhythm?
• Is there an underlying RBBB (Right Bundle Branch Block) or aberrant conduction?

Figure-1: The initial ECG in today's case — obtained from an older woman with acute dyspnea. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on Today's CASE:

The above questions were contemplated by initial providers in today's case. As to the rhythm in Figure-1 — the KEY is to avoid being sidetracked, and instead to remain systematic in our approach to today's tracing.

• PEARL #1: Whenever I am confronted by a challenging 12-lead ECG in association with a challenging arrhythmia — I always favor first at least taking a brief look at the rhythm in the long lead rhythm strip. This is because many of the questions we might have about the 12-lead — will often be answered once we appreciate what the underlying rhythm is.

PEARL #2: When confronted with an arrhythmia that contains 2 or more different elements — Begin with the easier-to-interpret element(s). Doing so often renders interpretation of the more difficult elements much simpler to understand. Often, the 1st "easier-to-interpret" element that I address will be to determine IF there is an underlying rhythm?

• For example, in Figure-1 — the muliple different QRS shapes (that we see in the long lead II rhythm strip at the bottom of the tracing) are difficult to assess.
• As a result, I defer looking at QRS morphology in the long lead II — and instead, I begin my interpretation by looking to see IF there is an underlying rhythm? In other words — Do we see P waves in the long lead II?

What do YOU think?

• Do we see P waves in the long lead II?

• NOTE: The answer appears below in Figure-2.

 

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Answer:

At 1st glance, on looking at the long lead II — I found it difficult to identify P waves until I arrived near the end of the rhythm strip.

• Then I saw the unmistakeable upright P wave in front of beat #17 (3rd RED arrow in Figure-2).
• And, once I saw this 1st upright P wave with a normal PR interval in front of beat #17 — it became easy to recognize the upright P wave in front of the next beat, albeit with a shorter PR interval (4th RED arrow in Figure-2).
• Now returning toward the front of the long lead II in Figure-2 — I was able to recognize the upright P waves (albeit with short PR intervals) in front of beats #7 and 8 (1st and 2nd RED arrows).

Figure-2: RED arrows in the long lead II rhythm strip highlight upright sinus P waves that I can readily identify.

Now take another LOOK at the long lead II in Figure-2. Can you identify any more P waves in this long lead rhythm strip?

• HINT: Use calipers! (Set your calipers to the P-P interval between any 2 consecutive P waves that we can readily identify = the P-P interval between either the first 2 — or the 3rd and 4th RED arrows in Figure-2).

• NOTE: The answer appears below in Figure-3.

 

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Answer:

I've highlighted with PINK arrows in Figure-3 — a series of small, upright (partially hidden) deflections that represent underlying "on time" sinus P waves at an atrial rate of slightly more than 100/minute. 

• Isn't it logical for there to be additional "on time" sinus P waves that I've not yet labeled in Figure-3?

• NOTE: The answer appears below in Figure-4.

Figure-3: I've labeled with PINK arrows a series of additional partially hidden upright sinus P waves.

 

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Answer:

It should now be apparent that an underlying rhythm of regular sinus P waves at a rate just over 100/minute is present throughout the entire long lead rhythm strip! My "color coding" in Figure-4 is as follows:

• The original 4 RED arrows represent the first 4 sinus P waves that were easiest to identify.
• PINK arrows in Figure-4 represent additional sinus P waves that I was able to identify by "walking out" the P-P interval that I had set my calipers to (Note partially hidden "on time" deflections highlighting the P waves under each of these PINK arrows).
• WHITE arrows in Figure-4 represent underlying "on time" sinus P waves that are all-but-certain to be present, albeit "hidden" by their simultaneous occurrence with either the QRS or T wave.
• 
  
• PEARL #3: Note that we have just established the presence of an underlying sinus P wave rhythm that for the most part is not related to neighboring QRS complexes. This is the definition of AV dissociation! — and the presence of AV dissociation during a regular wide tachycardia is virtually diagnostic of VT (See ECG Blog #133, among many other posts regarding the diagnostic value of AV dissociation). 

Figure-4: Colored arrows represent the underlying regular sinus rhythm that is present throughout today's tracing.

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Putting It All Together ...

Now that we've established the presence of a regular underlying sinus P wave rhythm with some element of AV dissociation — We can take another look at the multiple QRS shapes in the long lead II rhythm strip.

• Note in Figure-5 that there are 4 upright QRS complexes (albeit with slight variation in shape between beats #6,7; and #16,17) — and that the remaining 15 beats manifest negative QRS complexes. 
• Note also that I've added the labels, "C" and "F" to the long lead II rhythm strip in Figure-5.
• The KEY is beat #17. The QRS complex of this beat #17 is the most narrow beat, as well as the beat that is preceded by the most normal PR interval. This suggests that beat #17 is being conducted!
• And, if beat #17 is sinus-conducted — whereas beats #1-thru-5; #8-thru-15; and #18,19 all look very different (all being predominantly negative) with AV dissociation — this must mean that these predominantly negative beats represent an ongoing, underlying ventricular rhythm, occurring here at a rate of ~115/minute.

PEARL #4: As discussed in a number of blog posts (See ECG Blog #108, among others) — an independent ventricular rhythm at a rate of less than 120-130/minute is probably best classified as AIVR (Accelerated IdioVentriclar Rhythm) rather than "VT" (Ventricular Tachycardia). This is important clinically — because AIVR is often a consequence of other ongoing events, such that AIVR does not necessarily mandate immediate treatment with cardioversion.

• PEARL #5: The reason today's rhythm is "tricky" — is that the 15 predominantly negative QRS complexes in the long lead II rhythm strip do not "look" wide! But if we look directly upward at simultaneously-recorded leads V1,V2,V3 — the all-upright monophasic R wave in lead V1 for beats #11-thru-14 clearly looks to be ventricular in etiology.
• Thus, this is not RBBB and not aberrant conduction. Instead — there is underlying AIVR at ~115/minute. We prove this by the presence of AV dissociation. 
• Beat #17 is a "Capture" beat (labeled "C" in Figure-5).
• The reason the QRS morphology of beats #6,7 and 16 all look slightly different than that of beat #17 — is that these other upright QRS complexes all manifest different degrees of "Fusion" (labeled "F" in Figure-5) — with the concept of fusion beats explained in ECG Blog #128.
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• PEARL #6: The importance of recognizing Fusion and Capture beats — is that in association with underlying AV dissociation, this proves beyond doubt that the 15 predominantly negative QRS complexes in Figure-5 are ventricular beats!

Figure-5: I've labeled "Capture" and "Fusion" beats.

CASE Conclusion:

Today's patient was an older woman with diabetes — who presented with acute dyspnea. And although I do not have the specific details of what happened — I advised the following regarding clinical management:

• AIVR is often a well tolerated rhythm that does not necessarily mandate antiarrhythmic treatment or immediate cardioversion IF the patient is hemodynamically stable.
• Thus, if the reason for this patient's acute dyspnea is something "fixable" (ie, acute heart failure) — it may be reasonable to treat the heart failure. This may be all that is needed for the AIVR to resolve on its own.
• I do not see evidence of an ongoing acute infarction in Figure-5. To assess this — I focused on ST-T wave morphology of the more normally conducted beats (ie, the capture and fusion beats #16,17 in simultaneously-recorded leads V5,V6 — and the fusion beats #6,7 in simultaneously-recorded lead aVF). These complexes suggested marked LVH (greatly increased R wave amplitude for beat #17 in leads V5,V6) with ischemic symmetric T wave inversion in beats #6,7 and 16,17 in simultaneously-recorded leads aVF,V5,V6 — but no ST elevation.
• BOTTOM Line: If this patient remained hemodynamically stable — it may be reasonable to treat her heart failure (or other treatable cause of her acute dyspnea) to see if normal sinus rhythm returned. Depending on how the patient did, as well as depending on serial ECG and Troponin results — a decision can be made as the patient stabilized as to whether cardiac catheterization or other intervention will be needed. 

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Acknowledgment: My appreciation to Bashiruddin Sayeem  (from Chittagong, Bangladesh) for the case and this tracing.

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ECG Blog #536 — Why 2 Morphologies?

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 (with this most easily seen in leads II and III).
• 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 likely 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 is often a reperfusion arrhythmia in patients with 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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