Friday, August 22, 2025

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: 









Posted by ECG Interpretation at 10:27 PM

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