ECG Blog #493 — Why Did the Patient Faint?

The ECG in Figure-1 was obtained from an older man with diabetes — who reports a syncopal episode a few days earlier. No chest pain. Hemodynamically stable — and essentially asymptomatic at the time the ECG in Figure-1 was recorded.

QUESTIONS:

• How would you interpret the ECG in Figure-1?
• Does the 12-lead ECG help in diagnosis of the rhythm?

Figure-1: The initial ECG in today's case — obtained from an older man who reports a syncopal episode several days earlier. No chest pain! (To improve visualization — I've digitized the original ECG using PMcardio).

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MY Thoughts on the ECG in Figure-1:

Today's case provides an excellent example of how the various parts of this tracing combine to "tell a story".

• Looking first at the long lead II rhythm strip: The QRS is narrow — the overall heart rate is slow — P waves are present and look fairly regular — but for most of the tracing, every-other-P-wave is not conducted.
• PEARL #1: The simple step of labeling P waves facilitates appreciating non-conduction of every-other-P-wave (RED arrows in Figure-2).
• PEARL #2: The fact that the atrial rhythm is regular, but for most of the tracing alternate "on-time" P waves are not conducting — defines the rhythm in Figure-2 as some form of 2nd-degree AV Block.

Figure-2: I've labeled P waves in today's initial ECG with RED arrows. This facilitates seeing that the underlying atrial rhythm is regular.

PEARL #3: As emphasized below in the Audio Pearl and Video Pearl that appear below in ADDENDUM #2 — There are 3 Types of 2nd-degree AV Block:

• Mobitz I (which is also called AV Wenckebach) — in which the PR interval progressively increases until a beat is dropped (non-conducted).
• Mobitz II — in which the PR interval remains constant until one or more beats in a row are non-conducted.
• 2nd-degree AV Block with 2:1 AV Conduction — in which P waves are regular, but every-other-P-wave is non-conducted. Because we never see 2 P waves in a row that are conducted — we cannot tell if the PR interval would increase if given a chance to do so — which is why we simply call this block 2nd-degree with 2:1 AV conduction.
• KEY Point: In my experience — well over 90% of all 2nd-degree AV blocks are of the Mobitz I type! There are many variations of Mobitz I, in which escape beats, PACs, PVCs, echo beats, etc may make recognition of this conduction disturbance more difficult, which is why it is helpful to remember that the vast majority of 2nd-degree AV blocks that we encounter are of the Mobitz I type.

PEARL #4: When contemplating what type of 2nd-degree AV block may be present — it is helpful to remember that:

• If the QRS complex is narrow — the block is almost always Mobitz I (Mobitz II is a much more worrisome form of 2nd-degree AV block that occurs lower down in the conduction system — which is why the QRS is almost always wide with Mobitz II. Pacing is usually needed with Mobitz II).
• If there is evidence of inferior and/or posterior MI on the ECG — then the block is almost certain to be Mobitz I (as Mobitz I is a common complication of inferior and/or posterior MIs — that often resolves without need for pacing if reperfusion of the "culprit" artery is successfully restored).

PEARL #5: It is uncommon to switch back-and-forth between Mobitz I and Mobitz II. Therefore, if on review of rhythm monitoring — We see primarily 2:1 AV conduction, but also periods of typical Mobitz I (with an increasing PR interval until a beat is dropped) — then it becomes extremely likely that all periods of AV block in that patient represent Mobitz I.

• Isn't this what we see in Figure-2? Two P waves in a row are conducted (The RED arrows before beats #4 and 5 in Figure-2) — and the PR interval increases until a beat is dropped (ie, Beats #4 and 5 make up an AV Wenckebach cycle with 3:2 AV conduction).

LOOK at Figures-3, -4, and -5 — in which I've colored P waves to facilitate recognition of events. The laddergrams illustrate the mechanism of today's rhythm — which is 2nd-degree AV Block of the Mobitz I Type, with primarily 2:1 AV conduction — but also with 1 grouping of 3:2 AV conduction that confirms AV Wenckebach!

• RED arrow P waves in Figure-3 highlight P waves conducting with a constant PR interval (the PR interval being ~0.21 second — or at the upper limit of normal).
• YELLOW arrow P waves are non-conducted.
• The PR interval increases before beat #5 (highlighted by the BLUE arrow) — after which the next P wave is "on-time" but non-conducted, thereby completing a 3:2 Wenckebach cycle.

Figure-3: Colored arrows highlight 2:1 AV conduction with one 3:2 AV Wenckebach cycle.

Figure-4: Laddergram illustration of Figure-3.

Figure-5: Single-colored laddergram. The rhythm is 2nd-degree AV Block of the Mobitz I Type, with primarily 2:1 AV conduction — and 1 grouping with 3:2 AV conduction that confirms AV Wenckebach!

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Is There Evidence of Inferior and/or Posterior MI?

Keeping in mind PEARL #4 — I turned my attention to the 12-lead ECG. Despite the fact that today's patient did not report any CP (Chest Pain) — my "eye" was immediately drawn to the inferior leads (within the RED rectangles in Figure-6).

• Although baseline wander makes assessment of ST-T waves in leads II and III difficult — each of the inferior leads in Figure-6 manifest small q waves — ST segment straightening with slight ST elevation and a hyperacute appearance.
• Confirmation that these inferior lead ST-T wave findings are real — is forthcoming from the presence of reciprocal ST depression in lead aVL.
• Further confirmation of an ongoing acute event is forthcoming from the flat, "shelf-like" ST depression in leads V2,V3,V4 (BLUE arrows in these leads) — with this indicating associated posterior MI. 

PEARL #6: Awareness that the inferior and posterior walls of the left ventricle typically have a common blood supply — helps greatly when seeking to confirm an acute OMI ( = Occlusion-based Myocardial Infarction):

• Seeing subtle ST-T wave changes in all 3 inferior leads, as well as the ST flattening and depression that is maximal in leads V2,V3,V4 (as we do in Figure-6) — confirms acute infero-postero OMI until proven otherwise.
• As per PEARL #4 — the "story" that is told by today's initial ECG is completed by the finding of Mobitz I 2nd-degree AV Block for the rhythm.

PEARL #7: The story conveyed by ECG #1 tells us that today's patient did have a recent acute MI despite the absence of CP (ie, Today's patient had a "Silent" MI — as defined in the brief Audio Pearl below in today's ADDENDUM).

• This MI most probably occurred a few days earlier, at the time of this patient's syncopal episode — but despite bradycardia and the 2nd-degree AV Block seen in Figure-6, the patient was hemodynamically stable and essentially asymptomatic at the time this ECG was recorded. Nevertheless — Troponin was still elevated.

Figure-6: I've labeled leads highlighting the acute changes of acute infero-postero OMI.

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Today's CASE Continues:

Because the patient was admitted to a non-cath-capable hospital — initial treatment did not include angioplasty. The next morning — the repeat ECG shown in Figure-7 was obtained. The patient remained hemodynamically stable and essentially asymptomatic.

QUESTIONS: Regarding Figure-7:

• In light of clinical events in this case — How do you interpret the repeat ECG? 
• Does this repeat tracing suggest that treatment has been successful?
• Is the patient still in 2nd-degree AV Block in ECG #2?

Figure-7: Comparison between today's initial ECG — with the repeat ECG done the following morning.

ANSWERS: 

The rate of the rhythm in ECG #2 is clearly faster than it was in the initial tracing. I'll defer closer inspection of the rhythm for a moment — but at first glance, I see sinus-conducted beats but no non-conducted P waves.

• PEARL #8: The most time-efficient way to interpret serial ECGs — is to place both tracings side-by-side (as they are in Figure-7) — and to compare lead-by-lead — as well as to compare anatomic area by anatomic area. Unless you compare each tracing with the other tracing going lead-by-lead — it is all too easy to overlook subtle changes. 
• It is also much faster to compare tracings going lead-by-lead! (because you won't have to be going back-and-forth taking multiple looks because you forgot what some complexes look like).

In the limb leads:

• Compared to the 3 leads within the RED rectangles in the initial tracing — the ST elevation in the inferior leads looks less acute in ECG #2 (less straightening of the ST segment takeoff — and less J-point elevation). The terminal T wave inversion is now more pronounced, especially in lead III (which strongly suggests there has been some reperfusion of the "culprit" artery). The inferior Q waves are unchanged.
• Consistent with this suggestion of reperfusion in ECG #2 — is the increase in lead aVL of terminal T wave positivity (ie, the mirror-image opposite picture of the increased T wave inversion seen in lead III).

In the chest leads:

• The R wave in lead V2 is now clearly predominant. This earlier transition in the chest leads is consistent with evolution of posterior OMI (ie, positive Mirror Test — as described in ECG Blog #317).
• The most remarkable change in ECG #2 — is the evolution of chest lead T waves that have become taller, thinner and more symmetric, especially in leads V2,V3,V4,V5 (ie, positive Mirror Test — with this T wave appearance indicating posterior wall reperfusion).

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To facilitate assessment of the change in the cardiac rhythm between the 2 tracings in Figure-7 — I have put the long lead II rhythm strips from these tracings together in Figure-8.

• What do you see? 

Figure-8: Comparison of the rhythms in ECG #1 and ECG #2.

Comparison of the 2 Rhythm Strips in Figure-8:

As illustrated in Figures-3, -4, and -5 — the rhythm in the long lead II of ECG #1 is 2nd-degree AV Block of the Mobitz I Type, with primarily 2:1 AV conduction — but also with one 2-beat grouping with 3:2 AV conduction that confirms AV Wenckebach!

• The "good news" clinically — is that the 2nd-degree AV Block has resolved the following morning by the time ECG #2 was recorded!
• RED arrows in the long lead II rhythm strip in ECG #2 — indicate a fairly regular sinus rhythm for the first 6 beats, albeit with 1st-degree AV Block (PR interval ~0.24 second).
• Beat #7 in ECG #2 is a PAC (Premature Atrial Contraction) — with the small amplitude negative P wave before beat #7 clearly indicating a different atrial site of impulse formation ( = the ORANGE arrow in ECG #2).
• I suspect the 3 GREEN arrow P waves that follow beat #7 also originate from a different site in the atria — in that all 3 of these P waves are of similar size and shape to each other, and smaller than the first 6 RED arrow P waves. 

BOTTOM Line: Whether the change in P wave morphology that I describe above in ECG #2 represents a wandering atrial pacemaker, or simply a change in atrial focus resulting from the PAC — is uncertain.

• Regardless, the rhythm in ECG #2 is benign — and — this new rhythm represents significant improvement compared to ECG #1 because: i) The ventricular rate has increased, and is no longer bradycardic; and, ii) There is no longer 2nd-degree AV block.
• PEARL #9: The resolution of 2nd-degree AV Block in ECG #2 is yet one more sign (in addition to the reperfusion T waves described above in ECG #2) — that either through treatment or spontaneously, there has been a certain amount of reperfusion of the "culprit" artery (this point highlights the 2nd part of PEARL #4).

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Final CASE Follow-Up:

Cardiac cath was delayed in today's case until the patient could be transferred to a cath-capable facility. Results of cardiac catheterization and treatment interventions were as follows:

• 100% RCA occlusion and 90% narrowing of the proximal LAD (without other significant disease).
• An EF = 56% on Echo. 
• PCI to the RCA with IVUS (IntraVascular UltraSound) was performed — and staged PCI to the LAD was planned. The patient did well.

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Acknowledgment: My appreciation to Aarthi Natarajan (from Chennai, India) for the case and this tracing.

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ADDENDUM #1 (8/23/2025):

• For More Material — regarding ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria).

Figure-9: These are links found in the top menu on every page in this ECG Blog. They lead you to numerous posts with more on OMIs.

• In "My ECG Podcasts" — Check out ECG Podcast #2 (ECG Errors that Lead to Missing Acute Coronary Occlusion).
• In 'My ECG Videos" — Check out near the top of that page VIDEOS from my MedAll ECG Talks, that review the ECG diagnosis of acute MI — and how to recognize acute OMIs when STEMI criteria are not met (reviewed in ECG Blog #406 — Blog #407 — Blog #408).
• 
  
• Please NOTE — For each of the 6 MedAll videos at the top of the My ECG Videos page, IF you click on "More" in the description, you'll get a linked Contents that will allow you to jump to discussion of specific points (ie, at 5:29 in the 22-minute video for Blog #406 — you can jump to "You CAN recognize OMI without STEMI findings!" ).

P.S.: For a sobering, thought-provoking case discussed by cardiologist Dr. Willy Frick — with editorial Commentary by me at the bottom of the page (in the March 17, 2025 post) — Check out this case.

• As Dr. Frick and I highlight — not only is the current "STEMI paradigm" outdated — but in cases such as the one we describe, because providers waited until STEMI criteria were finally satisfied — cardiac cath and PCI were delayed for over 1 day.
• BUT — because the cath lab was activated within 1 hour of an ECG that finally fulfilled STEMI criteria — this case will go down in study registers as, "highly successful with rapid activation of the cath lab within 1 hour of the identification of a "STEMI". This erroneous interpretation of events totally ignores the clinical reality that this patient needlessly lost significant myocardium because the initial ECG (done >24 hours earlier) was clearly diagnostic of STEMI(-)/OMI(+) that was not acted on because providers were "stuck" on the STEMI protocol.
• The unfortunate result is generation of erroneous literature "support" suggesting validity of an outdated and no longer accurate paradigm.
• The Clinical Reality: Many acute coronary occlusions never develop ST elevation (or only develop ST elevation later in the course) — whereas attention to additional ECG criteria in the above references can enable us to identify acute OMI in many of these STEMI(-) cases.

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ADDENDUM #2 (8/23/2025):

• Below from ECG Blog #228 — a brief Audio Pearl on "Silent" MI.
• I've also included below an Audio Pearl — a Video Pearl — and links for download of PDFs reviewing the ECG diagnosis of AV Blocks.

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—  — 

ECG Media PEARL #44 (3:30 minutes Audio) — What is a "Silent" MI? — and How OFTEN do "Silent MIs" occur? (results from Framingham).

 

—  —

ECG Media PEARL #4 (4:30 minutes Audio): — takes a brief look at the AV Blocks — and focuses on WHEN to suspect Mobitz I.

My GOAL in the 15-minute ECG Video below — is to clarify ECG diagnosis of the 2nd-Degree AV Blocks, of which there are 3 Types:

• Mobitz I ( = AV Wenckebach).
• Mobitz II.
• 2nd-Degree AV Block with 2:1 AV conduction.

This 15-minute ECG Video (Media PEARL #52) — Reviews the 3 Types of 2nd-Degree AV Block — plus — the hard-to-define term of "high-grade" AV block. I supplement this material with the following 2 PDF handouts.

• Section 2F (6 pages = the "short" Answer) from my ECG-2014 Pocket Brain book provides quick written review of the AV Blocks (This is a free download).
• Section 20 (54 pages = the "long" Answer) from my ACLS-2013-Arrhythmias Expanded Version provides detailed discussion of WHAT the AV Bocks are — and what they are not!

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Review of the Ps, Qs, 3R Approach for systematic rhythm interpretation.
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 50 laddergram cases — many with step-by-step sequential illustration).
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• ECG Blog #164 — Which reviews step-by-step the diagnosis of a Mobitz I 2nd-degree AV block (with sequential laddergram illustration).
• 
  
• ECG Blog #168 — A complex dual-level AV Wenckebach (Laddergram).
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• ECG Blog #154 and ECG Blog #55 and ECG Blog #224 and ECG Blog #232 — Acute MI with AV Wenckebach.
• 
  
• ECG Blog #63 — Mobitz I with Junctional Escape Beats.
• ECG Blog #344 — Mobitz I vs II vs neither ...
• ECG Blog #416 — Another OMI & AV Block ...
• ECG Bog #472 — Another AV Block ...

ECG Blog #492 — Confused by the Pacemaker

Today's patient is an older man with a permanent pacemaker that was placed ~1 year ago for complete AV Block. He presents to the ED (Emergency Department) at this time — for new CP (Chest Pain) that began earlier in the day, and which has still persisted. The patient was hemodynamically stable at the time the ECG in Figure-1 was recorded.

QUESTIONS:

• How would you interpret the ECG in Figure-1?
• Should the cath lab be activated?

Figure-1: The initial ECG in today's case.

My Thoughts on Today’s CASE:

We are told that today's patient has a pacemaker — and that he presents for new CP persisting over the course of a day. Questions that arise include the following:

• Do we see evidence of this patient's pacemaker in ECG #1?  If so — Is the pacemaker working appropriately?
• Can we assess the ECG of a patient with a pacemaker for ST-T wave changes of acute OMI? If so — Are there any worrisome findings in ECG #1?

ANSWERS: Can We Detect Acute OMI in a Paced Tracing? 

As seen in Figure-2 — Pacemaker spikes are present (within the small RED circles in leads V4,V5). Similar tiny spikes are intermittently seen in other leads.

• At least in leads V4,V5 — we see these pacemaker spikes just before wide QRS complexes with a LBBB-like morphology — so the pacmaker appears to be appropriately capturing the ventricles at ~85/minute.
• It is at least sometimes possible to assess a paced ECG for ST-T wave changes of acute ischemia. Such assessment is made more challenging by QRS widening of paced beats (and resultant altered ST-T wave morphology) — but there are times when we can see evidence of acute OMI on a completely paced tracing.
• In such instances — application of Smith-Modified Sgarbossa Criteria help to identify abnormal ST-T wave findings despite complete pacing (See Pearl #4 in ECG Blog #282 for review of Smith-Modified Sgarbossa Criteria).

PEARL #1: Even more than applying Smith-Modified Sgarbossa Criteria — I favor assessing for acute ischemia in paced tracings by looking for ST-T wave changes that just should not be there! This should be readily evident in Figure-2:

• There is no way that the 4+ mm of downsloping ST depression in lead V6 with terminal T wave positivity can be a "normal" finding (within the RED rectangle in Figure-2). If anything — we would expect secondary ST-T wave changes of LBBB or in a paced tracing to be oppositely directly to the predominantly negative QRS deflection in lead V6.
• In the context of this clearly abnormal downsloping ST depression in lead V6 — the more subtle flattened ST depression in neighboring lead V5 (BLUE arrow in this lead) is also abnormal.
• The next lead in Figure-2 to catch my "eye" — is lead V1 (within the BLUE rectangle) — as the relative amount of J-point ST elevation in this lead is clearly disproportionate to the modest size of the S wave in this lead (The relative amount of ST elevation in lead V1 does appear to satisfy the 25% criteria of Modified-Smith Sgarbossa Criteria outlined in ECG Blog #282).
• Given the clearly abnormal ST elevation in lead V1 — I thought the J-point ST elevation in neighboring lead V2 was also abnormal. While not satisfying the 25% criterion of Smith-Modified Sgarbossa — the J-point in this V2 lead is angled sharply (BLUE arrow in V2) — rather than manifesting a smoother transition as is normally expected between J-point and ST segment (Note the much smoother transition between J-point and ST segment in neighboring leads V3,V4 that I interpreted as normal).

BOTTOM Line: While the ST-T wave changes I describe above for leads V2 and V5 in Figure-2 are admittedly subtle — in this older patient with new CP — the abnormally shaped and disproportionate amount of ST depression in lead V6, supported by the disproportionate amount of ST elevation in lead V1 — has to indicate acute OMI until proven otherwise!

• PEARL #2: The presence of coved ST elevation in leads V1,V2 with clearly abnormal ST depression in leads V5,V6 is consistent with Precordial Swirl — which suggests a proximal LAD occlusion (See ECG Blog #380 for more on Precordial Swirl).
• To address the question posed at the beginning of today's case: YES, the cath lab should be immediately activated given the history of new CP and the ECG findings in Figure-2.

Figure-2: I've labeled today's initial ECG.

The CASE Continues:

A prior tracing on today's patient was found. To facilitate comparison in Figure-3 — I've put this previous ECG from ~8 months earlier together with today's initial ECG.

• Does availability of this prior ECG support your decision to activate the cath lab?

Figure-3: Comparison between today's initial ECG — and a previous ECG done ~8 months earlier.

Comparison with the Prior Tracing:

Availability of the prior ECG on today's patient removes all doubt about the need to activate the cath lab!

• PEARL #3: The BEST way to hone your ECG interpretation skills — is to train your "eye" in recognizing subtle findings by follow-up comparison with subsequent tracings to see how more subtle findings on the original tracing evolved over time.
• Lead-to-lead comparison between ECG #1 and ECG #2 in Figure-3 shows significant changes in virtually every lead!
• Looking first at the 2 leads that made the diagnosis for us — it is easy to see how abnormal the ST-T waves in leads V5 and V1 of Figure-1 truly were!
• Looking further at the more subtle changes in leads V2 and V5 that I highlighted above — we can confirm the validity of my observations on seeing that there was more ST elevation in lead V2 in ECG #1 than there was on the prior ECG — and the subtle, flattened ST depression in lead V5 of ECG #1 was not at all present on the prior ECG.
• ST-T wave changes in other leads are present on comparison between the 2 tracings in Figure-3 — but those changes are not nearly as easy to detect — which confirms my PEARL #4 from today's case = It is usually more difficult to assess paced tracings for acute ischemia — but it is definitely not impossible.

CASE Conclusion:

The cath lab was activated. Cardiac cath revealed the following:

• There was significant 3-vessel disease.
• 90% distal stenosis of the LMain.
• 50% mid-LAD stenosis.
• 90% patent ostial stenosis of the LCx.
• 50% mid-RCA stenosis.

The LMain narrowed area was successfully stented to the patent LAD. The patient did well in follow-up.

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PEARL #5: Had I not been told — I may not have realized that today's patient had a pacemaker from the initial ECG shown in Figure-1. Pacemaker spikes are often difficult to detect for a number of reasons:

• There could be pacemaker malfunction.
• There could be signal interference and artifact and/or "noise".
• Modern pacemakers increasingly use bipolar leads — and bipolar leads generate smaller spikes on ECG.
• Filter settings are suboptimal. This is especially true when the low-pass filter is set below the standard value of 150 Hz. That said — even at 150 Hz, the percentage of patients whose pacemaker spikes will be visible on a standard ECG has been found to be far less than the percentage for detecting pacemaker spikes on ECG with a higher low-pass filter of 300 Hz (Sun et al — Chin Med J 132(5):534-541, 2019).

Regarding Filter Settings:

I suspect suboptimal Filter settings is the most common reason that pacemaker spikes are not readily seen on many tracings. All too often — filter settings are ignored. 

• Different settings are typically used for monitoring when emphasis is placed on rhythm determination vs diagnostic mode, for which the focus is on interpreting 12-lead waveforms. 
• Greater filtering is generally used in monitor mode, with a common setting between 0.5 Hz and 40 Hz. Doing so has the advantage of minimizing artifact and baseline wander that may affect rhythm interpretation. 
• In contrast — a broader passband (typically from 0.05 Hz to 150 Hz) — is recommended for diagnostic mode, where more accurate ST segment analysis is essential.
• Modern bipolar pacemakers generate smaller pacing spike amplitudes compared to older devices, making them harder to detect on the ECG. Awareness that the filter setting is important — especially if you find yourself hopelessly looking for spikes in a tracing of a patient thought to have a pacemaker.

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Acknowledgment: My appreciation to 林柏志 (from Taiwan) for the case and this tracing.

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ECG Blog #491 — VT until Proven Otherwise?

The ECG in Figure-1 was obtained from an older man with a history of coronary disease and chronic AFib (Atrial Fibrillation) — who was admitted acutely ill to the ICU (Intensive Care Unit) for septicemia. He was hemodynamically stable at the time this tracing was recorded.

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NOTE: The ECG in today's case looks similar to the tracing I presented a few weeks ago in ECG Blog #489. But is the answer the same?

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QUESTIONS:

• How would you interpret the ECG in Figure-1?
• How certain are you of your diagnosis?
• Did the fact that this patient was hemodynamically stable at the time this ECG was recorded influence your diagnosis?
• How would you treat this patient?

Figure-1: The initial ECG in today's case — obtained from an older man being treated in the ICU for septicemia. (To improve visualization — I've digitized the original ECG using PMcardio).

My Thoughts on Today’s CASE:

Applying the Ps, Qs and 3Rs (See ECG Blog #185) — the rhythm in Figure-1 is fast (~220/minute) — regular — with a wide QRS — and without clear sign of atrial activity. This defines the rhythm as a regular WCT (Wide-Complex Tachycardia). As per the LINKS to other cases that are found at the bottom of this page — the principal differential diagnosis is between:

• VT (Ventricular Tachycardia) — or —
• SVT (SupraVentricular Tachycardia) with either of the following: i) Preexisting BBB (Bundle Branch Block); or ii) Aberrant conduction as a result of the rapid rate.

On rare occasions — "something else" (ie, hyperkalemia, sodium channel blocker toxicity — or other toxicity) may result in a regular WCT rhythm. Given that this patient has been hospitalized in the ICU — presumably he is not hyperkalemic, such that the main consideration is to distinguish between VT vs SVT with either preexisting BBB or rate-related aberrant conduction. 

KEY Points to consider include the following:

• Statistically, in an unselected adult population — at least 80% of regular WCT rhythms without sign of atrial activity will turn out to be VT. Given that today's patient is an older adult with known coronary disease — the likelihood of VT is increased to ~90% even before we consider specific features of this ECG.
• QRS morphology may allow for greater precision in predicting WCT etiology — especially IF ECG features predictive of either VT or SVT are present. That said, even in cases in which QRS morphology is suggestive — it is rare to attain 100% certainty prior to our need to begin treatment.
• Hemodynamic stability during the WCT rhythm does not rule out VT. While true that patients with sustained VT are much more likely to decompensate than those who remain in a persistent SVT rhythm — these generalities do not always hold true. If LV function is good and the heart rate is not excessively rapid — then some patients in sustained VT may remain hemodynamically stable for a period of hours (or even longer).

What About Today's CASE?

When this case was sent to me — I found it surprising that this acutely ill patient with septicemia would be hemodynamically stable in this WCT rhythm — because the heart rate is so  very rapid (ie, ~220/minute).

• I thought the rhythm was fascicular VT — because QRS morphology resembled rbbb conduction in the chest leads (ie, with an all upright complex in lead V1 — an RS pattern in lateral lead V6 with terminal negativity consistent with rbbb-like conduction — and marked rightward axis deviation in the frontal plane).
• Given this patient's acutely ill status and the very rapid rate of his WCT rhythm — I probably would have moved to synchronized cardioversion. However, because this patient was hemodynamically stable — providers at the bedside reasonably opted for a trial of IV Amiodarone, being ready to cardiovert at any if time the patient became hemodynamically unstable.

PEARL #1: For as much as the rhythm in Figure-1 "looks" like VT — it's important to appreciate the limitations of our diagnostic accuracy from this single ECG. Confounding ECG features on this tracing include: 

• i) Lack of a clear triphasic rsR' pattern in lead V1 (instead there is an rR' pattern in lead V1 without descent of any S wave below the baseline — as illustrated in Figure-4 in the ADDENDUM below); 
• ii) Despite predominant negativity of the QRS in all 3 standard limb leads (leads I,II,III) — the lack of an all-negative QRS in either lead I and/or lead aVF means that we can not rule out a supraventricular rhythm (instead there is a tiny initial positive deflection in lead I and in each of the inferior leads); 
• iii) Lack of a completely monophasic R wave in lead aVR negates the value of this lead for predicting VT (instead there appears to be a tiny q wave = an initially negative deflection in this lead); 
• iv) Despite predominant negativity of the QRS in lateral chest lead V6 — the lack of an all negative QRS in lateral lead V6 negates the value of this lead for predicting VT (instead there is a small but-definitely-present initial R wave in this lead).

PEARL #2: Although each of the above ECG findings in PEARL #1 make a supraventricular rhythm less likely — none of them guarantee that the rhythm is VT. We need to remember that much of the time we will not be able to be certain if a regular WCT rhythm is VT or SVT at the time that we need to begin our treatment. Instead — we often need to formulate our best hunch as to what we think the rhythm is likely to be — and base our treatment decisions accordingly.

PEARL #3: Finding a prior ECG on this patient could prove invaluable — because if QRS morphology during the patient's baseline rhythm looks the same as during the WCT — this could prove that the WCT is not VT. 

• Unfortunately in today's case — this patient's baseline 12-lead ECG could not be found at the time it was needed.

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The CASE Continues:

Within minutes of beginning IV Amiodarone — the ECG shown in the bottom panel of Figure-2 was obtained. The patient remained hemodynamically stable.

QUESTIONS:

• What is learned from comparison of today initial ECG — with the repeat ECG obtained within minutes after beginning IV Amiodarone?

Figure-2: Comparison between the initial ECG — with the repeat ECG obtained within minutes of starting IV Amiodarone.

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ANSWER:

Surprisingly, the very rapid WCT rhythm seen in today's initial ECG has dramatically slowed in ECG #2 to another regular, wide rhythm.

• Comparing QRS morphology during the WCT rhythm ( = the upper tracing in Figure-1) — with QRS morphology shortly after initiation of IV Amiodarone — Isn't QRS morphology in virtually every lead remarkably similar?

PEARL #4: ECG features in ECG #2 now look much more in favor of an SVT with aberrant conduction because: 

• i) Lead V1 in ECG #2 now manifests a typical triphasic morphology for supraventricular conduction because there is a small initial r wave — followed by an S wave that descends below the baseline — that finishes with a tall, pointed terminal R' ( = a taller "right rabbit ear" ).
• ii) The tiny initial r waves that we barely saw in ECG #1 — are now much more evident (and much more consistent with supraventricular conduction with RBBB/LAHB).
• iii) Leads V4,V5 and especially V6 in ECG #2 — now manifest significantly taller narrow R waves that are strongly suggestive of a supraventricular rhythm.

KEY Point: Despite the above morphologic features of ECG #2 that strongly suggest a supraventricular rhythm — P waves are not seen! As a result — I was not yet certain that the rhythm in ECG #2 was now supraventricular.

• PEARL #5: Did you notice that the rate of the regular wide rhythm in ECG #2 is almost half that of the initial rapid WCT rhythm? — almost as if ECG #1 represented a reentry SVT rhythm, that as a result of the AV nodal blocking effect of Amiodarone — was now only conducting every-other-impulse to the ventricles.
• Alternatively — the rhythm in ECG #2 could represent junctional tachycardia with preexisting RBBB/LAHB. Although an automatic junctional tachycardia is not a common rhythm in adults — today's clinical situation (ie, a "sick" patient with multiple underlying disorders) is perhaps the most common setting in which we encounter fast junctional rhythms.

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The CASE Continues:

Since the patient remained hemodynamically stable with the rhythm in ECG #2 — IV Amiodarone was continued. A few minutes later — the rhythm in ECG #3 was observed.

• To facilitate comparison in Figure-3 — I've put the 3 ECGs in today's case together.

QUESTION:

• What do we learn from ECG #3?

Figure-3: Comparison of the 3 ECGs in today's case.

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ANSWER:

The rhythm in ECG #3 is faster than it was in ECG #2 — and is now irregularly irregular without P waves. This patient with a known history of chronic AFib — is now back in AFib with a rapid ventricular response. The 5th beat in leads V1,V2,V3 that is wider and different in morphology from the rest of the tracing is a PVC.

• Treatment of this patient with IV Amiodarone was effective! Although the end result of this treatment is still suboptimal (ie, recurrence of this patient's chronic AFib — now with a rapid ventricular response) — the "good news" is that: i) The rate of the rhythm in ECG #3 is slower than it was in ECG #1; and, ii) We now know that the rhythm in ECG #1 was not VT (because AFib is a supraventricular rhythm and QRS morphology in ECG #3 is virtually identical to QRS morphology during ECG #1).

CASE Follow-Up.

• Comparison of QRS morphology in the 3 tracings shown in Figure-1 was found to be the same as this patient's QRS morphology in prior baseline tracings. This confirms that the initial ECG in today's case was not VT. 
• Instead — today's initial rhythm most likely represents a reentry SVT in which QRS widening is the result of preexisting RBBB/LAHB.
• This patient continued to have a stormy course — but seemed to be gradually improving over time as his septicemia was treated. His AFib is chronic. Rate control will hopefully be optimized once his underlying conditions improve.
• 
  
• Editorial Comment: What I especially liked about this case — is that it keeps us humble. I truly thought the initial ECG was VT. But "not all patients read the textbook" — and over time, serial ECGs confirmed a supraventricular etiology (with preexisting RBBB/LAHB). Truly — we often have to begin treatment of wide tachycardias before we are certain of the rhythm etiology. A trial of IV Amiodarone was reasonable given hemodynamic stability of the patient — and providers were able to confirm a supraventricular etiology.

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Acknowledgment: My appreciation to Andrea D'Angelo (Naples, Italy) for allowing me to use this case and these tracings.

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ADDENDUM (8/9/2025):

Figure-4: QRS morphology in lead V1 that suggests a supraventricular etiology (from my ACLS Pocket Brain-2013).

 

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Additional Relevant ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Reviews my System for Rhythm Interpretation, using 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.
• 
  
• ECG Blog #220 — Review of the approach to the Regular WCT (Wide-Complex Tachycardia).
• ECG Blog #489 — in which the initial ECG looks similar to that in today's case (but for which the answer is different).
• ECG Blog #196 — Reviews another regular WCT.
• 
  
• ECG Blog #263 and Blog #283 — Blog #361 — Blog #384 — and Blog #460 — and Blog #468 — More WCT Rhythms ...
• 
  
• 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).
• 
  
• 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.
• 
  
• 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 — more regular WCTs.
• ECG Blog #475 — Aberrant SVT?
• 
  
• 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.
• 
  
• ECG Blog #133 and ECG Blog #151— for examples in which AV dissociation confirmed the diagnosis of VT.
• 
  
• 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. 
• A series of 3 challenging tracings with QRS widening (See My Comment at the bottom of the page in the March 6, 2025 post on Dr. Smith's ECG Blog).
• 
  
• 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.