ECG Blog #463 — Lots to Explain ...

I was sent the ECG shown in Figure-1 — told only that this tracing was obtained prior to elective electric cardioversion of a patient who had long been in persistent AFlutter (Atrial Flutter).

• Serum electrolytes were normal at the time of cardioversion.
• The patient tolerated cardioversion well — and later that day was discharged from the hospital. (The post-cardioversion tracing will be shown momentarily in Figure-3).
• Unfortunately — additional clinical details regarding today’s case are not known (nor is it known what medications the patient may have been taking).

QUESTIONS:

• How to interpret today’s initial rhythm? (shown in Figure-1).
• Why is the QRS wide? 

Figure-1: The initial ECG in today's case (obtained prior to elective electrical cardioversion).

My Thoughts on the ECG in Figure-1:

Limb leads and chest leads in Figure-1 show 2 short (~5 second) and somewhat different-looking rhythm strips.

• There is definite group beating in the limb leads (groups of 2 beats with alternating long-short cycles) — but no such organization in the chest leads.
• Very rapid and regular atrial activity is seen in a number of chest leads and limb leads (best seen in lead II — as highlighted by RED arrows in Figure-2). The P-P interval is slightly more than 1 large box in duration — which corresponds to an atrial rate just under 300/minute (and defines the underlying rhythm as AFlutter).
• As is often the case with AFlutter — flutter waves are well seen in some leads (ie, leads II,III,aVF; V1,V2) — but not in others.
• The QRS is wide — with a morphology consistent with LBBB (Left Bundle Branch Block) conduction in the chest leads (predominantly negative in anterior chest leads — and all positive in lead V6). 

QUESTIONS:

• Why is there group beating in the limb leads?
• Why no group beating in the chest leads?
• If there is LBBB conduction in the chest leads — Why is the QRS all negative in lead I?

Figure-2: RED arrows highlight very rapid and regular atrial activity in lead II. Atrial activity is also seen in leads III,aVF; V1 and V2.

The CASE Continues:

I then saw the repeat ECG obtained after cardioversion.

• Does this repeat ECG in Figure-3 provide answers to some of the above questions?

Figure-3: The repeat ECG obtained after cardioversion.

My Thoughts on the Repeat ECG in Figure-3:

Sinus rhythm has been restored following cardioversion. The overall heart rate is slow — and the QRS for most beats is now narrow.

• To facilitate interpretation of Figure-3 — I've numbered the beats and have labeled atrial activity in Figure-4.

Figure-4: I've labeled the post-conversion tracing.

The Post-Conversion Tracing:

Limb leads and chest leads in Figure-4 are continuous.

• RED arrows highlight sinus P waves in this brady rhythm (heart rate a bit under 50/minute).
• BLUE arrows highlight the presence of 2 PACs (Premature Atrial Contractions). Of interest — the QRS complex is wide in Figure-4 only for these 2 PACs ( = beats #2 and #7). Note that QRS morphology for both of these early beats is consistent with LBBB conduction (monophasic all upright R wave in leads I and aVL for beat #2 — and for beat #7, there is predominant negativity in the chest leads until the all upright R wave in lead V6).
• PEARL #1: The fact that the QRS was consistently wide during the faster rhythm (ie, while the patient was in AFlutter) — but now in Figure-4 shows a normal (narrow) QRS complex with the underlying post-conversion rhythm of sinus bradycardia except for the 2 early-occurring beats (beats #2 and 7, which are PACs) — suggests that the reason for QRS widening in the initial ECG is likely to reflect rate-related LBBB aberration (See ECG Blog #242 for more on rate-related BBB).
• PEARL #2: Did you notice in the post-conversion tracing that there is ST segment coving with fairly deep T wave inversion in the chest leads? In view of the clinical history (ie, that this patient had a history of longstanding AFlutter — but as far as we know, no chest pain) — this ST-T wave change most likely reflects a "memory" effect, in which there will often be ST-T wave abnormalities that persist for hours (up to a few days) following a long period of a sustained tachycardia. (Clinical correlation, and possibly Troponin levels — are needed to determine whether this deep T wave inversion needs additional evaluation).

QUESTIONS:

Take a LOOK at Figure-5 — in which I've put the initial ECG together with the repeat ECG recorded after cardioversion.

• Does this comparison in Figure-5 confirm why despite QRS widening with LBBB conduction in the chest leads of the initial ECG — the QRS complex in lead I of this tracing is all negative? (HINT: Look also at what happens to QRS morphology in lead aVR of ECG #1 compared to the appearance of lead aVR in ECG #2).
• P.S.: Did you figure out why there is group beating in the limb leads of the initial ECG?

Figure-5: To facilitate comparison — I've put the initial ECG together with the post-cardioversion tracing.

ANSWERS:

• Answering the 2nd question first — it is common with AFlutter for there to be group beating similar to that seen in the limb leads of ECG #1. As I'll illustrate momentarily in a step-by-step laddergram derivation (in Figures-8 thru -13) — this group beating is usually the result of dual-level Wenckebach conduction out of the AV Node. It is most often not the result of a pathological AV block — since normal 1:1 AV conduction usually returns with resumption of sinus rhythm.
• As to the lack of group beating for the 5 second rhythm in the chest leads — I interpreted this simply as AFlutter with a variable ventricular response. This probably occurred as a result of changing conduction ratios out of the dual levels within the AV Node.
• 
  
• Finally — The all negative QRS complex in lead I of the initial ECG is the result of LA-RA lead reversal!

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QUESTION:

• How do we know there is lead reversal in ECG #1?

ANSWER (Looking at the ECGs in Figure-5):

The technical misadventure of lead reversal is more common than is commonly appreciated. Of the lead reversals — the most common (by far) is a mix-up of the LA (Left Arm) and RA (Right Arm) electrodes. When this happens — lead I resembles the QRST appearance normally seen in lead aVR — and vice versa.

• PEARL #3: Standard lead I is a left-sided lead. Since the heart lies toward the left — predominant electrical activity will almost always be directed toward the left. Even in the setting of a large lateral infarction — it is rare to see a predominant Q wave in lead I. Yet in ECG #1 — the QRS complex is all negative in lead I. Although possible for this to occur (ie, with a very unusual conduction defect) — Think dextrocardia or LA-RA lead reversal if you see an all-negative QRS in lead I.
• P.S.: We know that the all negative QRS in lead I is not the result of dextrocardia — because R wave progression in the chest leads of ECG #1 is exactly as expected for LBBB conduction (and R wave progression would be reversed if there was dextrocardia).

Additional confirmation of LA-RA reversal in ECG #1:

• Lead aVR is a right-sided lead. In the absence of marked RVH — One would not expect to see the all positive QRS that we see in lead aVR of ECG #1. But if lead I looked like lead aVR looks (and lead aVR looked like lead I looks) — then ECG #1 would look exactly as expected for this patient who manifests typical LBBB conduction in the chest leads.
• Lead V6 is a left-sided chest lead. Given that lead V6 is all positive in ECG #1 — We would not expect the QRS complex in left-sided lead I to be all negative!
• Final proof of LA-RA reversal is forthcoming in ECG #2. Note that beat #2 (which is the 1st PAC in this tracing that conducts with LBBB aberration) — now manifests typical LBBB morphology, with an all upright QRS in both lead I and lead aVL (within the dotted BLUE rectangle in Figure-5).

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What would ECG #1 look like IF there was not LA-RA reversal?

• I review multiple other examples of lead reversal in ECG Blog #396. As these example show — we can "correct" for the effects that each type of lead reversal has on the ECG (See Figure-6):

Figure-6: Correcting for the effects of LA-RA lead reversal.

And now substituting what ECG #1 would have looked like if all limb leads were correctly positioned — Take a LOOK at Figure-7 !

Figure-7: This is how Figure-5 would look — IF we correct for LA-RA reversal that was present in the initial ECG.

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Laddergram Illustration: Today's Dual-Level Wenckebach ...

I conclude today's case with laddergram derivation of the group beating pattern that we see in the limb leads of ECG #1.

• Figure-8 shows the rhythm I'll review. This is the 5-second lead II rhythm strip with flutter waves highlighted by RED arrows (taken from Figure-2).

Figure-8: RED arrows highlight flutter waves in this lead II excerpt from Figure-2. Note the group beating (alternating longer-shorter R-R intervals for beats #1-2; 3-4; 5-6). Note also the identical PR intervals that precede beats #3,5,7.

Figure-9: Laddergram STEP-1. It is usually easiest to begin a laddergram by filling in the Atrial Tier. BLUE arrows show the onset of P waves (in this case, flutter waves) as my reference point for drawing in atrial activity. Because conduction through the atria is generally rapid — I drew in near-vertical lines in the Atrial Tier.
=  =  =  =  =
NOTE: Because I suspected dual-level AV block within the AV Node — I have divided the AV Nodal Tier into 2 parts (by drawing in a horizontal BLACK dotted line).

Figure-10: Laddergram STEP-2. I next fill in the Ventricular Tier.
 BLUE arrows show the onset of each QRS complex as my reference point for each of the QRS complexes in this tracing. 
=  =  =  =  =
KEY Point: The "EASY part" for constructing most laddergrams consists of these first 2 STEPS (that are shown in Figures-9 and -10). Now the challenge begins — for trying to "solve" the laddergram by figuring out which of the P waves (in this case, flutter waves) in the Atrial Tier are being conducted to the ventricles.

Figure-11: While realizing that many complex tracings may have more than a single potential laddergram explanation — I find postulating 2:1 AV conduction in the upper AV Nodal level most often works for me when contemplating AFlutter with dual-level Wenckebach conduction.
= = = = =
KEY Point: Because of "concealed conduction" — flutter waves that are very close to a QRS complex are usually not able to conduct to the ventricles. For example — the 3rd RED arrow in this Figure-11 is unlikely to be conducting. As a result — flutter waves before-and-after this 3rd RED arrow probably are able to conduct through at least the upper AV Nodal level (PINK lines in this upper AV Nodal level).
This leaves me with the BLUE-lined path as the most logical conduction passageway to produce beat #3.

Figure-12: Continuing to postulate 2:1 conduction through the upper AV Nodal level once again suggests this next BLUE-lined path as the most logical conduction passageway to produce beat #4.

Figure-13: The pattern of beats repeats. My completed laddergram suggests the solution — which is AFlutter with dual-level conduction out of the AV Node (ie, with 2:1 conduction out of the upper AV Nodal level — and 3:2 Wenckebach conduction through the lower level).
NOTE: This pattern that we see for the first 6 beats changes for beat #7 — as there is no 2nd beat in this last grouping.

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Final PEARL #4: 

To remember: It is very common to see group beating with AFlutter — and — there will often be dual-level AV block of these rapid flutter waves out of the AV Node.

• Even without having to draw a laddergram — we can quickly recognize dual-level Wenckebach conduction out of the AV Node by seeing group beating that occurs in association with consecutive non-conducted flutter waves (as is evident in Figure-8) — especially when there are identical PR intervals before many of the beats.
• The "good news" — is that these consecutive non-conducted flutter waves generally do not represent a fixed (pathologic) form of AV block! Instead — normal 1:1 AV conduction usually resumes once AFlutter is converted to sinus rhythm.

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Acknowledgment: My appreciation to Samuel K. Sørensen (from Copenhagen, Denmark) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs, 3R Approach.
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 100 laddergram cases — many with step-by-step sequential illustration).
• 
  
• ECG Blog #264 — Reviews LA-RA Lead Reversal.
• ECG Blog #396 — for a list of lead reversals ...

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• ECG Blog #259 — Reviews step-by-step laddergram for a patient with Dual-Level AV Block.
• ECG Blog #243 — Reviews a case of AFlutter with Dual-Level Wenckebach out of the AV Node.
• ECG Blog #226 — Works through a complex Case Study (including an 11:00 minute ECG Video Pearl that walks you through step-by-step in the constrution of a laddergram with Wenckebach conduction and duallevel block within the AV Node).
• ECG Blog #416 — Case Study of acute OMI with step-by-step illustration of dual-level AV Wenckebach.
• ECG Blog #347 and Blog #439 — more examples of dual-level AV block.

 

ADDENDUM (1/3/2025): 

—  —

ECG Media PEARL #71 (5:45 minutes Audio) — Reviews the phenomenon of Dual-Level Wenckebach out of the AV Node (HOW to recognize this phenomenon — and how to distinguish it from Mobitz II).

 

ECG Blog #462 — Why so Slow ... ?

I was sent the ECG in Figure-1 — told only that the patient was an older adult who reported dizziness with activity.

QUESTIONS:

• What is the rhythm? (HINT: There are at least 4 important findings that should be noted).
•   — Is there AV block?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on Today’s CASE:

In general — I favor beginning my assessment of a 12-lead ECG with a long lead rhythm strip by first taking a quick LOOK at the rhythm before proceeding with my interpretation of the 12-lead ECG. As always — I favor the Ps, Qs, 3R Approach (See ECG Blog #185):

• Starting with the long lead II (at the bottom of today’s tracing in Figure-1) — the ventricular rhythm is slow but Regular (ie, with a constant R-R interval of just over 8 large boxes in duration — corresponding to a ventricular Rate just under 40/minute).
• The QRS is narrow in all 12 leads — which defines the rhythm either as supraventricular (ie, arising from at or above the AV Node), or in the Bundle of His (ie, The QRS would be wide if the rhythm originated from outside the conduction system in ventricular myocardium). 
• Regarding P waves — Atrial activity is present, albeit not in the form of P waves. Instead — Figure-2 highlights the presence of a regular “sawtooth” pattern at a rate of ~300/minute (ie, the interval between each sawtooth deflection being approximately 1 large box in duration). Thus, the underlying Rhythm in today’s tracing is AFlutter (Atrial Flutter).

The final parameter in the Ps,Qs,3R Approach — is to assess the 3rd “R” (ie, If P waves or other sign of atrial activity is present — Is this atrial activity Related to neighboring QRS complexes?).

• The most time-efficient way to determine IF one or more P waves are Related to neighboring QRS complexes — is to look in front of each QRS complex, and to ask yourself IF atrial activity manifests a fixed relationship to neighboring QRS complexes.
• No such “fixed” relationship seems to exist in Figure-2 — since the distance between the last “sawtooth” flutter wave and the next QRS complex to appear continually varies. That is, unlike AFlutter with dual-level Wenckebach conduction out of the AV Node (as appears in ECG Blog #243) — the coupling interval between the last atrial deflection before the QRS complex that ends the relative pause is never the same.
• In support of our suspicion that none of the flutter waves in Figure-2 are being conducted to the ventricles — is the regular and very slow rate of the ventricular rhythm (ie, New, untreated AFlutter most often manifests 2:1 AV conduction — with a ventricular rate that is close to 150/minute).

IMPRESSION: The underlying rhythm in today’s case is AFlutter with complete (3rd-degree) AV block, and a very slow escape rhythm at ~40/minute.

• Since the QRS complex is narrow in all 12 leads of this ECG — the escape rhythm originates from either the AV node or the Bundle of His.
• Unless a potentially “fixable” cause of this rhythm can be found (ie, acute ischemia from recent infarction; electrolyte disturbance, use of rate-slowing medication) — the patient will need a pacemaker.
• And, if other causes of this rhythm are ruled out (ie, acute/recent ischemia — rate-slowing medication — severe electrolyte or acid-base disturbance — hypothyroidism — sleep apnea) — then given older age of this patient, the diagnosis will almost certainly be SSS (Sick Sinus Syndrome — See ECG Blog #342).

Figure-2: I’ve labeled regular atrial activity in today’s tracing (RED lines) — that manifests an atrial rate of ~300/minute.

What About the 12-Lead ECG?

Now that we have interpreted the rhythm in today’s tracing — What about the 12-lead ECG?

• The frontal plane Axis in Figure-2 does not make sense! This is because: i) Standard leads I,II,III suggest a nearly vertical axis of at least +80 degrees (equally large positive deflections in leads II and III — with no more than a tiny QRS in lead I ) — whereas this would make the all negative QRS in lead aVF impossible!; — and, ii) QRS morphology in all 3 augmented leads (aVR,aVL,aVF) is all negative and looks nearly identical — which is also impossible given the findings in standard leads I,II,III. Therefore — some form of technical misadventure (ie, lead misplacement) is present — and the ECG should be immediately repeated.
• The chest leads show extremely poor R wave progression (ie, No more than a tiny initial r wave in leads V1,V2 and V3). This suggests that at some point in time — that this patient may have had anteroseptal infarction (which clearly is an important consideration given the rhythm of very slow AFlutter with complete AV block).
• Leads V4,V5,V6 — all show 1 mm of flat ST depression. This strongly suggests ischemia — which could be recent and a contributing (or precipitating) cause of today’s abnormal rhythm.

Unfortunately — I do not have follow-up for this case. Nevertheless, this case provides a wonderful illustration of multiple abnormal findings.

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Acknowledgment: My appreciation for the anonymous submission of today's case.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #185 — My Ps, Qs, 3R System for Rhythm Interpretation.
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 100 laddergram cases — many with step-by-step sequential illustration).

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• 
  
• ECG Blog #164 and ECG Blog #251 —Review of Mobitz I 2nd-Degree AV Block, with detailed discussion of the "Footprints" of Wenckebach.
• ECG Blog #236 — Reviews in our 15-minute Video Pearl #52 how to recognize the 2nd-Degree AV Blocks (including "high-grade" AV block). 
• ECG Blog #186 — Reviews when to suspect 2nd-Degree, Mobitz Type I.
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• ECG Blog #404 — Walks you through a step-by-step approach to this AV block case (with links to a VIDEO of this case, and to Blog #344 for more details).
• 
  
• ECG Blog #352 — emphasizes that 1st-degree AV block with a very long PR interval may have hemodynamic consequences.
• 
  
• ECG Blog #243 and ECG Blog #347 — Examples of AFlutter with dual-level AV block (Wenckebach) out of the AV Node.

 

ECG Blog #461 — STEMI, LV Aneurysm or Neither?

I was sent the ECG shown in Figure-1 — initially without the benefit of any history.

• How would you interpret this tracing?
•    — What is YOUR differential diagnosis of this tracing?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

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The Obvious Concern:

• I immediately realized the reason that I was sent this tracing: ==> there is ST elevation in the anterior chest leads!

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MY Initial Thoughts on Figure-1:

Looking systematically:

• There is a regular sinus rhythm at ~85/minute (upright P waves in lead II — with a constant and normal PR interval).
• The QRS is narrow (ie, not more than 1/2 a large box in duration).
• The QTc is at most borderline prolonged.
• The Axis is markedly leftward, as per a predominantly negative QRS complex in lead aVF. Criteria for LAHB (Left Anterior HemiBlock) are fulfilled — given the predominantly negative QRS in lead II (ie, indicating a frontal plane axis more negative than -30 degrees).

Regarding Chamber Enlargement:

• Criteria for atrial enlargement are absent (Reviewed in ECG Blog #75). So, although there is a negative component to the terminal P wave in lead V1 — I favor undercalling LAA because of limited specificity for this amount of P wave negativity in V1 as an indication of LAA.
• That said — voltage for LVH is markedly increased!

There is marked LVH:

• I've reviewed criteria for LVH on many occasions (See ADDENDUM below — for review of LVH criteria that I favor — as well as ECG Blog #73 for full discussion).
• As per Figure-5 (in the Addendum below) — S wave amplitude is markedly increased in today's ECG (attaining an S wave depth = 28 mm in lead V2 — and an S wave depth = 28 mm in lead V4 — as shown in Figure-2).
• 
  
• PEARL #1: Sometimes with LVH — instead of seeing tall R waves with LV "Strain" in the lateral chest leads — we see the "mirror-image" opposite picture in right-sided leads V1,V2 (ie, LVH may be manifested by deep anterior S waves — with ST elevation in leads V1,V2 and/or V3). This is precisely what we see in today's case!

Figure-2: Assessment of R wave and S wave amplitude in the chest leads is rendered difficult by marked overlap of complexes in several leads. To facilitate assessment — I've colored in selected R waves and S waves.

Completing our Systematic Approach (with Q-R-S-T Changes):

• Q Waves — There is a tiny septal q wave in lead aVL — which is unlikely to be important. But there are large QS waves in anterior leads V1,V2,V3.
• R Wave Progression — Because of these large QS waves in the anterior leads, there is poor R wave progression (with Transition delayed until between leads V5-to-V6).
• ST-T Waves — I've drawn in the PR segment baseline in leads V1,V2,V3 of today's ECG to highlight the amount of ST elevation (RED arrows in Figure-3 indicating the J-point as the marker for judging the amont of ST elevation).
• Elsewhere, the 3 inferior leads and lead V6 show nonspecific ST-T wave flattening. Finally, lateral leads I and aVL show subtle, shallow T wave inversion — which is consistent with a "strain equivalent" pattern (as I highlight in Panel B of Figure-6 in today's Addendum).

Figure-3: I've labeled the PR segment baseline and J-points in selected chest leads to highlight the amount of ST elevation.

Putting It All Together:

Today's ECG shows a sinus rhythm at ~85/minute — a borderline QTc — LAHB — marked LVH — and — QS waves in leads V1,V2,V3, with no more than a tiny r wave in lead V4 — plus, ST elevation that begins in lead V1 and extends through to lead V5. Clinically — this may indicate any of the following (See Figure-4):

• i) Antero-Septal MI may have occurred at some point in time — as suggesed by QS waves in leads V1,V2,V3.
• 
  
• ii) That there is marked LVH is strongly suggested by the greatly increased chest lead QRS amplitudes (with S waves = 28 mm in leads V2 and V4 — as shown in Figure-4) — with a "strain equivalent" pattern in lateral leads I and aVL (BLUE arrows in these leads).
• The anterior lead ST elevation may simply reflect LV "strain" in a patient with marked LVH, which when manifest by deep anterior S waves (rather than tall lateral R waves) — may produce a vector in which the hypertrophied, posterior-lying left ventricle opposes normal anterior forces, thereby reducing (and sometimes eliminating) anterior r waves.
• PEARL #2: As shown within the RED insert in Figure-4 — In such cases, the ST-T wave changes of LV "strain" (that are usually seen in lateral leads) — may present a mirror-image opposite ST-T wave picture of "strain" in anterior leads. This may account for the anterior ST elevation seen in today's case (BLUE arrows in leads V1,V2,V3).
• 
  
• iii) There could be acute LAD (Left Anterior Descending) coronary Occlusion that is now superimposed on the ECG of a patient with longstanding LVH, perhaps with also previous anterior infarction.
• 
  
• iv) The findings in Figure-4 could reflect LV aneurysm.

Conclusion: As I contemplated today's tracing that I initially interpreted without the benefit of any history — I thought any of the above diagnostic possibilities might be present. Although I suspected that the ECG findings in Figure-4 were not acute — I was not at all certain of that suspicion from this single ECG.

• Clearly — a detailed history would be needed for adequate clinical assessment. Does this patient have a history of cardiac disease? Did the patient have CP? (Chest Pain). If so — When did the CP begin? Was CP still present at the time that the ECG in Figure-4 was taken?
• Can we find a previous ECG on this patient (looking to determine if the QS waves and ST elevation is new or old).
• Especially if CP was ongoing — a repeat ECG is needed (looking for signs of acute evolution) — in addition to Troponins, Echo and further assessment until we can determine if an acute process is in progress. 

Figure-4: I've labeled KEY findings in today's ECG.

CASE Follow-Up:

I later learned the history in today's case — which was that a middle-aged man with diabetes and hypertension — who presented to the ED (Emergency Department) for abdominal pain that had awakened him from sleep.

• The patient was markedly hypertensive in the ED — but he did not have CP.
• Chest X-Ray was normal. 
• Troponins were negative.
• Echo showed significant LVH with normal LV function and no wall motion abnormality.
• Radionuclide scan was negative for ischemia.
• Previous ECGs were found in the patient's chart — which showed similar findings of marked LVH with anterior ST elevation attributed to LV "strain".
• 
  
• In Summary: The patient's abdominal pain was treated. An acute cardiac event was ruled out. Cardiac cath was not done.

"Take Home" Message: Anterior lead ST elevation does not necessarily indicate acute infarction when the patient has LVH that is manifest by deep anterior S waves. In such cases — the anterior ST elevation may simply reflect LV "strain" (as per the "Mirror Test" that is shown within the RED insert in Figure-4).

• Further evaluation may be needed in such cases to clarify what may be "new" vs "old" (ie, To rule out a new acute event that could be superimposed on longstanding LVH).
• KEY Point: Anterior ST elevation is unlikely to represent LV "strain" if anterior S waves are not larger than is usually expected (ie, if there is no LVH). 

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Acknowledgment: My appreciation for the anonymous submission of today's case.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation. 
• 
  
• ECG Blog #73 — Reviews "My Take" on the ECG Diagnosis of LVH. 
• ECG Blog #92 — Presents another perspective for ECG Diagnosis of LVH.
• ECG Blog #424 — Another example of when marked LVH may manifest anterior ST elevation.
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• For cases similar to today, in which LVH may mimic ischemia — Check out My Comment at the bottom of the page of the following posts in Dr. Smith's ECG Blog — the November 29, 2023 post — June 20, 2020 — March 31, 2019 — March 29, 2019 — and the December 27, 2018 post.
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• ECG Blog #218 — Reviews HOW to define a T wave as being Hyperacute? 
• ECG Blog #230 — Reviews HOW to compare Serial ECGs (ie, "Are you comparing Apples with Apples or Oranges?"). 

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ADDENDUM (12/21/2024): I've added below in Figure-5 and Figure-6 additional material to facilitate ECG diagnosis of LVH and LV "strain".

 

Figure-5: The voltage and other criteria I favor for ECG diagnosis of LVH (Please see ECG Blog #73 for additional details).

Figure-6: Illustration and description of LV “strain” and a “strain equivalent” pattern (See text).

ECG Blog #460 — A Wide Tachycardia ...

I was sent the ECG in Figure-1 — initially told only that it was obtained from an older man with “palpitations”.

• The cardiology team thought the rhythm was an SVT (SupraVentricular Tachycardia) — with QRS widening as a result of aberrant conduction.

QUESTION:

• Do YOU agree that the rhythm is consistent with an SVT, in which there is QRS widening because of aberrancy?
• How would you treat this patient?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

The ECG in Figure-1 — shows a regular WCT ( = Wide-Complex Tachycardia) at ~160/minute, without clear sign of atrial activity.

• Clinically — The 1st priority in assessing this patient would be to determine hemodynamic status! (because IF this patient was unstable with this ECG — then regardless of what the rhythm happens to be — synchronized cardioversion would become immediately indicated).
• On the other hand — IF the patient is completely stable with this rhythm, then by definition — You have at least a “moment of time” to more thoroughly contemplate the etiology of this rhythm.

PEARL #1: As emphasized in many other blog posts (ie, ECG Blog #220 and Blog #196, to name just two) — the differential diagnosis of a regular WCT rhythm without clear sign of atrial activity should be assumed to be VT (Ventricular Tachycardia) until proven otherwise.

• Taking all comers in an unselected adult population — statistical likelihood that a regular WCT without atrial activity will be VT is at least 80%.
• If the patient is at least middle-aged, and especially if there is a history of underlying heart disease — then statistical likelihood that a regular WCT without atrial activity will be VT increases to ~90%. To Emphasize — This is a 90% likelihood of VT even before you look at the ECG!
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• In Today's CASE — All that we initially knew was that the patient was an "older adult" — but we were not told if he had underlying heart disease. So before looking at QRS morphology — statistical odds were ~80% likelihood of VT.

PEARL #2: Assessment of the frontal plane axis and consideration of QRS morphology in the 12-lead tracing during the WCT rhythm can increase (or decrease) statistical likelihood of VT from our initial estimate of ~80% (See ADDENDUM below for user-friendly criteria I favor for this purpose).

• Finding extreme axis deviation in the frontal plane during the WCT would strongly favor VT. 
• To Emphasize: By “extreme” axis deviation — the QRS must be entirely negative in either lead I or lead aVF. Even a small positive deflection in either of these leads negates the reliability of this criterion. 
• In Today's CASE — The 12-lead tracing in Figure-1 does not satisfy this “extreme” axis deviation criterion — because the axis is normal (ie, The net QRS deflection is positive in both leads I and aVF — therefore the axis lies between the normal range of 0-to-90 degrees). 

Perhaps the most helpful criterion for assessing QRS morphology during a regular WCT rhythm — is whether QRS morphology resembles a typical conduction block? (ie, typical RBBB; typical LBBB — or bifascicular block with either RBBB/LAHB or RBBB/LPHB).

• As emphasized in ECG Blog #204 — Focus on the 3 KEY leads ( = leads I,V1,V6) facilitates recognition of RBBB and LBBB within seconds. That said — whereas somewhat atypical QRS morphology does not necessarily indicate VT  — the finding of a completely typical QRS morphology for RBBB or LBBB may greatly increase the likelihood of a supraventricular rhythm.

In Today's CASE — QRS morphology is very atypical for either RBBB or LBBB. As a result — the WCT rhythm in Figure-1 has to be assumed VT until proven otherwise!

• ECG #1 is not consistent with LBBB — because while the QRS is all positive in lead V6, there is no predominant negativity in the anterior leads.
• ECG #1 is not consistent with RBBB — because: i) Lead V1 lacks a triphasic morphology; — ii) Lateral leads I and V6 lack any terminal S wave; — and, especially because: iii) The QRS is almost all positive in all 6 chest leads (there is no more than a tiny initial q wave in leads V3,V4,V5).

PEARL #3: If ever there is concordance of QRS complexes in all 6 chest leads (ie, all 6 chest leads are either entirely positive or entirely negative) — this is virtually diagnostic of VT.

• The sensitivity of this criterion not good — such that it will be rare that you will see positive or negative QRS concordance in all 6 chest leads during a regular WCT rhythm. That said, if ever you do — then you have essentially made the diagnosis of VT. 
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• In Today's CASE — Those tiny initial q waves in leads V3,V4,V5 mean that positive concordance is not strictly present. That said — given how tiny these 3 precordial q waves are, I interpreted the almost all positive QRS in leads V1-thru-V6 as supportive of presumed VT (albeit not diagnostic).
• The only exceptions that I'm aware of to the above-cited morphologic criteria for VT are: i) IF the rhythm is antidromic AVRT — in which case the impulse travels forward over an AP (Accessory Pathway) in a patient with WPW, therefore resulting in a regular WCT rhythm that resembles VT (For more on the various arrhythmias in patients with WPW — See ECG Blog #18); — ii) If the baseline ECG during sinus rhythm manifests a widened and very abnormal QRS morphology as a result of prior infarction, cardiomyopathy and/or preexisting bundle branch block; — and, iii) If there is some toxicity (such as hyperkalemia) which widens and distorts QRS morphology.
• Conclusion: Assuming none of the above exceptions exist — the ECG in Figure-1 has to be presumed VT until proven otherwise. 

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CASE Conclusion:

Today's patient was hemodynamically stable in association with the ECG in Figure-1.

• In view of this patient's hemodynamic stability — medical therapy was initially tried. There was no response to vagal maneuvers, nor to 3 doses of Adenosine. This was followed with several Amiodarone boluses — again with no response.
• Some clinical history was obtained — which revealed that the patient has known coronary disease (S/P CABG — with ejection fraction of ~35%).

At this point — the cardiology team still suspected a supraventricular etiology for today's rhythm. That said, plans were made for synchronized cardioversion given lack of response to medical treatment. Before this could be done — the patient spontaneously converted to sinus rhythm.

Final Reflections on Today's CASE:

• The ECG in Figure-1 strongly suggests VT. That said — clinicians often need to begin treatment before they are 100% certain of the rhythm diagnosis. In today's case — a trial of medical therapy was reasonable since the patient was hemodynamically stable.
• It's important to appreciate that the odds that today's rhythm was VT immediately increased as soon as it was learned that the patient has significant underlying heart disease.
• Given that multiple doses of antiarrhythmic medication were given — there should have been adequate time in this patient with known significant coronary disease — to obtain a prior ECG. This could have been insightful if a prior tracing were to show a preexisting conduction defect in sinus rhythm with the same QRS morphology as seen in Figure-1. 
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• While nothing is 100% — the sequence and choice of treatment options should be influenced by relative probability of the differential diagnosis.
• Several doses of Adenosine were given in today's case. This drug is extremely effective for converting reentry SVT rhythms. It may also convert a certain number of patients with idiopathic VT. That said, by definition — today's patient does not have idiopathic VT, because he has known coronary disease. (See ECG Blog #197 — for review of idiopathic VT).
• Although the effects of Adenosine wear off within 30-90 seconds, and most patients tolerate this drug surprisingly well — Adenosine is not benign (See ECG Blog #402). As a result — I would not have risked using Adenosine in today's case ( = my opinion) given virtual nil chance of it working.
• That said — the fact that both vagal maneuvers and 3 doses of Adenosine failed to convert today's rhythm is yet more evidence in favor of VT.
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• IV Amiodarone (bolus and drip) — is an appropriate medication to try in today's case, given that this patient was hemodynamically stable. An advantage of this medication — is that it may be effective for both VT and SVT rhythms. As I lack full details from today's case — I do not know if it ultimately was the Amiodarone that converted today's WCT to sinus rhythm.
• IF the decision is made for a trial of medical therapy — the provider should stay at the bedside, ready to immediately cardiovert if at any time during the treatment process the patient's hemodynamic status deteriorates.
• Alternatively — a decision could have been made to sedate the patient and immediately cardiovert, given the 90+% likelihood of VT in this patient with known coronary disease.
• While important to engage in thoughtful discussion about cases like this — ultimately, "Ya gotta be there" to know which therapeutic option(s) might be best, given the particulars of any given case. I offer the above as retrospective reflection to stimulate discussion on actions to consider.
• My understanding is that the decision was made for today's patient to be formally evaluated by EP cardiology — with consideration given to ablation and/or insertion of an ICD (Implantable Cardioverter Defibrillator).
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• For more on evaluation and management of the regular WCT — See the ADDENDUM below.

 

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Acknowledgment: My appreciation for the anonymous submission of this case.

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Additional Relevant ECG Blog Posts to Today’s Case:

• ECG Blog #185 — Reviews my System for Rhythm Interpretation — with use of the Ps, Qs & 3R Approach.
• ECG Blog #210 — Reviews the Every-Other-Beat (or Every-Third-Beat) Method for estimation of fast heart rates — and discusses another case of a regular WCT rhythm. 
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• ECG Blog #422 and Blog #425 — Cases with Congenital Heart Disease in Adults.
• ECG Blog #220 — Review of the approach to the regular WCT ( = Wide-Complex Tachycardia).
• ECG Blog #196 — Another Case with a regular WCT.
• ECG Blog #263 and Blog #283 — Blog #361 — and Blog #384 — More WCT Rhythms ...
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• ECG Blog #197 — Reviews the concept of Idiopathic VT, of which Fascicular VT is one of the 2 most common types. 
• ECG Blog #346 — Reviews a case of LVOT VT (a less common idiopathic form of VT).
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• ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 
• ECG Blog #203 — Reviews ECG diagnosis of Axis and the Hemiblocks. For review of QRS morphology with the Bifascicular Blocks (RBBB/LAHB; RBBB/LPHB) — See the Video Pearl in this blog post.
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• ECG Blog #211 — WHY does Aberrant Conduction occur?
• ECG Blog #301 — Reviews a WCT that is SupraVentricular! (with LOTS on Aberrant Conduction).
• ECG Blog #445 and Blog #361 — Another regular WCT rhythm ...
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• ECG Blog #323 — Review of Fascicular VT.
• ECG Blog #38 and Blog #85 — Review of Fascicular VT.
• ECG Blog #278 — Another case of a regular WCT rhythm in a younger adult.
• ECG Blog #35 — Review of RVOT VT. 
• ECG Blog #42 — Criteria to distinguish VT vs Aberration.
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• ECG Blog #133 and ECG Blog #151— for examples in which AV dissociation confirmed the diagnosis of VT.
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• Working through a case of a regular WCT Rhythm in this 80-something woman — See My Comment in the May 5, 2020 post on Dr. Smith’s ECG Blog. 
• Another case of a regular WCT Rhythm in a 60-something woman — See My Comment at the bottom of the page in the April 15, 2020 post on Dr. Smith’s ECG Blog. 
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• Review of the Idiopathic VTs (ie, Fascicular VT; RVOT and LVOT VT) — See My Comment at the bottom of the page in the September 7, 2020 post on Dr. Smith’s ECG Blog.
• Review of a different kind of VT (Pleomorphic VT) — See My Comment in the June 1, 2020 post on Dr. Smith’s ECG Blog.

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ADDENDUM (12/13/2024):

• I've reproduced below from ECG Blog #361 — a number of helpful figures and my Audio Pearl on assessment of the regular WCT rhythm.

 

Figure-2 : My LIST #1 = Causes of a Regular WCT (Wide-Complex Tachycardia) of uncertain Etiology (ie, when there is no clear sign of sinus P waves).

Figure-3: Use of the "3-Simple Rules" for distinction between SVT vs VT.

Figure-4: Use of Lead V1 for assessing QRS morphology during a WCT rhythm.

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ECG Media PEARL #13a (12:20 minutes Audio) — reviews “My Take” on assessing the regular WCT (Wide-Complex Tachycardia), when sinus P waves are absent — with tips for distinguishing between VT vs SVT with either preexisting BBB or aberrant conduction.