ECG Blog #472 — At Least 4 Major Findings

The ECG in Figure-1 was obtained from a middle-aged man — who presents to the ED (Emergency Department) with 6 hours of chest pain. He is hemodynamically stable.

QUESTION:

• As per the title of this blog post — How many important findings can you identify?

Figure-1: The initial ECG in today's case — obtained from a middle-aged man with 6 hours of chest pain. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on ECG #1:

Time-efficient assessment is KEY when your patient presents with new CP (Chest Pain). The decision of whether or not to activate the cath lab must be made quickly for optimal benefit. In today's case, once you learn that the ECG in Figure-1 is from a man with new CP — it should take less than 1 minute to know that the cath lab should be activated. What follows below reflects "My 1-minute Survey" of the ECG in Figure-1:

• Since this patient presents with CP — I initially focused my attention on the 12-lead, looking first to see if there was an obvious MI. Doing so — My "eye" was immediately drawn to the 3 inferior leads — each of which show significant ST elevation (RED arrows in Figure-2). As a side note — there is also suggestion of terminal T wave inversion (best seen in the 3rd QRS complex in lead III — and to a lesser extent in lead aVF).
• PEARL #1: In a patient with new CP, confirmation that inferior lead ST elevation is the result of acute MI is immediately forthcoming — IF there is reciprocal ST depression in lead aVL. The BLUE arrow in lead aVL confirms that this mirror-image opposite ST-T wave picture of reciprocal ST depression is present. Thus, the total time it should take to confirm an ongoing acute inferior MI in this patient with new CP should ideally be less than 30 seconds (just enough time to look at leads II,III,aVF and lead aVL). As a result, even before looking we look at the rest of this tracing — We already know that the cath lab should be activated.
• PEARL #2: The fact that there is ST elevation in lead III > lead II (in association with marked reciprocal ST depression in lead aVL) — strongly suggests acute RCA (Right Coronary Artery) occlusion as the "culprit" artery. And although identifying the probable "culprit" artery is an advanced point — it does have clinical relevance here, since the RCA supplies the RV (Right Ventricle) — but the LCx (Left Circumlflex) does not (See PEARLS #4,5 below).
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• PEARL #3: Knowing there is an acute inferior STEMI — I looked next to see if there is also acute posterior involvement (which so often accompanies inferior MI). To do this, I focused on lead V2 — which shows: i) Early transition (The R wave in lead V2 is already much taller than the S wave is deep in this lead); — and, ii) Shelf-like ST segment flattening (if not downsloping), with abrupt angulation at the onset of an acute-looking T wave that appears to be overly peaked. This confirms acute posterior MI.
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• PEARL #4: Note in neighboring lead V1 that there is no ST depression. Instead, the ST segment in lead V1 is coved and slightly elevated — which in association with suspected acute RCA occlusion, strongly suggests acute RV involvment!
• PEARL #5: When a free moment is found — right-sided leads should be obtained to confirm acute RV MI. In the meantime — sublingual nitroglycerin is best avoided, as its vasodilator effect may precipitate hypotension in volume-dependent RV infarction. Be ready with prudent administration of IV fluids if blood pressure drops (See ECG Blog #190 — for more on RV MI, and its different hemodynamics).

Figure-2: The first leads to catch my "eye".

The Long Lead II Rhythm Strip:

Given that we are told today's patient was hemodynamically stable at the time of his initial ECG — I initially paid less attention to the long lead II rhythm strip in Figure-1.

• And — We now already know that this patient with new CP has an ongoing infero-postero MI (and that prompt cath is indicated).

At this point — I looked closer at the rhythm (Figure-3): 

• With the exceptionn of beat #5 — there is group beating in the form of repetitive 2-beat groups with an alternating pattern of shorter and longer R-R intervals of similar duration.
• The QRS is narrow.
• P waves are present — but many of these P waves are not conducted.
• PEARL #6: Common things are common! In the setting of an acute inferior MI — group beating with short pauses and non-conducted P waves will almost always turn out to be AV Wenckebach ( = 2nd-degree AV block of the Mobitz I Type). 

Figure-3: Turning our attention for a quick look at the rhythm.

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To Emphasize: All of the above findings that I have discussed should be identified within your 1st minute of looking at today's initial ECG.

• Ideally — the cath lab would now be activated.

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Taking a Closer LOOK at the Initial ECG: 

There is more going on in today's initial ECG. With cardiology ideally already being consulted (hopefully with plans for prompt cardiac catheterization) — and, with the patient hopefully still hemodynamically stable — there should be a moment for more thorough assessment (See Figure-4 below):

• Looking closely at lead V6 — slight ST elevation is also seen here. Thus, there is ongoing infero-postero-lateral MI (with probable RV involvement — pending confirmation with right-sided leads).
• Although ECG criteria for LVH are not satisfied — I thought LVH is likely given generous R wave amplitudes in leads V3,V4,V5 (albeit QRS amplitudes often fluctuate with ongoing infarction — so Echo obtained at some later point after stabilization would be the test to assess for chamber size and function).
• ST-T waves were relatively flat in the mid-chest leads. While not altering the immediate plan for this patient (which should be for prompt cath, presumably with PCI for the occluded RCA) — this nonspecific ST-T wave flattening made me wonder if this patient had multi-vessel disease.
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• PEARL #7: The small and narrow q waves in lateral chest leads V5,V6 seemed likely to represent "normal septal q waves". But — larger-than-expected Q waves in each of the inferior leads (especially in lead III) — are probably the result of this patients ongoing acute inferior STEMI.
• The surprisingly tall R wave already in lead V2 is probably the posterior wall equivalent of these inferior lead Q waves (Most patients with acute posterior MI do not yet manifest early transition with tall anterior R waves on their initial ECG). These inferior lead Q waves and the early transition tall R wave in lead V2 are probably markers of this patient's ongoing MI that began ~6 hours earlier with the onset of his CP.
• The "good news" — is that the earlier-noted suggestion of terminal T wave inversion in leads III and aVF (as well as the terminal T wave positivity in lead aVL) — may be signs that spontaneous reperfusion of the "culprit" artery is beginning to occur. Regardless — given ongoing CP and persistent ST elevation, prompt cath with PCI is still immediately indicated!
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• PEARL #8: We can quickly "hone in" on a more specific diagnosis of the rhythm in Figure-4. Doesn't the simple act of labeling P waves make it so much easier to recognize the relationship between each P wave and it's neighboring QRS complex? What do YOU think?

Figure-4: I've labeled P waves with RED arrows — which now makes the underlying regular sinus rhythm obvious.

More on the Initial Rhythm in Figure-4:

As noted earlier in PEARL #6 — We should suspect AV Wenckebach ( = 2nd-degree AV block of the Mobitz I Type) within seconds of seeing the initial ECG since the inferior STEMI is obvious and — "Common things are common!"

• In the setting of acute inferior MI — Group beating with short pauses and non-conducted P waves will almost always turn out to be AV Wenckebach.
• Labeling P waves (as we have done in Figure-4) should allow us to immediately recognize that the identical PR interval is seen before each QRS that ends each of the short pauses (ie, We see the same normal PR interval before beats #1,3,5,6,8 and 10).
• Focusing within each of the 2-beat groups — it should be apparent that the 2nd PR interval within each group is increasing (The PR interval before beats #2,4,7,9 and 11 is longer than the PR interval before beats #1,3,6,8 and 10).
• Each Wenckebach cycle then completes with non-conduction of the P waves after beats #2,4,5,7,9 and 11.

Laddergram of Figure-4:

The above relationships are easier to appreciate by review of the laddergram that I've drawn in Figure-5.

• RED arrows highlight normal sinus P waves that conduct with a normal PR interval the 1st beat in each of the groups.
• The 2nd P wave in each group is conducting with longer PR interval (BLUE arrows before beats #2,4,7,9 and 11).
• YELLOW arrows highlight on-time sinus P waves that fail to conduct because of the block. The rhythm is 2nd-degree AV Block of the Mobitz I Type — with predominantly 3:2 AV conduction (since all but one of the groups have 3 on-time sinus P waves, of which only 2 of these P waves are conducting).
• The single QRS beat #5 manifests 2:1 AV conduction (ie, There are 2 on-time sinus P waves — but only 1 of these P waves conducts).

Figure-5: Laddergram of today's rhythm (See above text).

Is Treatment of the Rhythm Indicated?

• There are times that Atropine is an effective treatment, or at least temporizing measure for 2nd-degree, and even 3rd-degree AV block. This is especially true during the early hours of acute inferior MI (during which time parasympathetic tone is likely to be increased, and therefore more responsive to Atropine).
• Atropine is much less likely to be effective if the QRS complex is wide — since this suggests a lower level of AV block (Atropine is most effective when AV block is at the level of the AV node — as it usually is with inferior MIs in which the QRS is narrow).
• However, Atropine is not benign. While its action improves AV conduction — it may increase the sinus rate, producing a sinus tachycardia with adverse effect. Thus, use of this drug should be reserved for patients with Mobitz I or narrow-QRS 3rd degree AV blocks from acute inferior MI in which the patient is hemodynamically unstable because of the AV block. 
• Atropine is not indicated in today's case because: i) We are told this patient is hemodynamically stable; — ii) The overall ventricular rate in Figure-5 is not bradycardic; — and, iii) Prompt cath with PCI is the treatment of choice for today's patient. There is an excellent chance that the AV block will quickly resolve following PCI.

Should Morphine be given for this Patient's CP?

• In the past — Morphine was routinely given to patient's with acute CP. This practice is no longer routinely advised until a definitive treatment decision has been made. Once you know that prompt cath is needed (or in the absence of cath capability — once you begin to treat with thrombolytics) — then relief of the patient's CP with morphine or other medication assumes high priority. For example, in today's case — as soon as the interventionist agrees on the need for prompt cath — Morphine can be given! (and, as discussed above — the need for prompt cath in today's case should be made within minutes).
• In contrast — if you (and your consulting cardiologist) are uncertain about the need for prompt cath with PCI — then Morphine is best avoided until you become certain about your treatment decision. This is because early use of Morphine may mask symptoms — and this has been shown to delay definitive treatment with PCI or thrombolytics. 
• For this reason — it's essential to expedite the diagnostic process. Time is myocardium. In a patient with worrisome new CP — if definitive diagnosis of acute OMI is not forthcoming from the initial ECG — the repeat the ECG within 15-20 minutes, and continue with frequent serial ECGs, troponins and close clinical monitoring until you can confidently determine IF the patient is (or is not) having ongoing infarction.

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Acknowledgment: My appreciation to Abdullah Al Mamun (from Dhaka, Bangladesh) for the today's case and this tracing.

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ADDENDUM #1 (3/8/2025) — regarding the Term "OMI"

The new terminology that I favor adds "OMI" ( = Occlusion-based Myocardial Infarction) to the classification of acute MI. This is in recognition of the clinical reality that at least 1/3 of all acute coronary occlusions do not manifest a sufficient amount of ST elevation to qualify as a "STEMI" (and many OMIs do not manifest any ST elevation at all — despite cath proven coronary occlusion).

• Many of these acute OMIs are readily identifiable on ECG (as I've demonstrated in countless posts on this ECG Blog — as well as in Dr. Smith's ECG Blog).
• Comparable benefit from acute reperfusion (by PCI or thrombolysis) is seen in patients with acute coronary occlusion from an OMI, as from a STEMI. As a result — my GOAL is to "spread the word" to as many clinical providers as possible — that attention to a limited number of clinical parameters can rapidly increase clinician ability to recognize acute OMIs (without wasting precious time that risks losing viable myocardium in the fruitless wait for ST elevation that may never occur).

NOTE: As shown in Figure-6 — I've added tabs to the top menu of every page in my ECG Blog for easy access LINKS to material emphasizing the above concepts related to early recognition and treatment of acute OMI when millimeter-based STEMI criteria are not satisfied.

• 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).
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• 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!" ).

Figure-6: 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.

ADDENDUM #2 (3/8/2025):

• I've included below an Audio Pearl — a Video Pearl — and links for download of PDFs reviewing the ECG diagnosis of AV Blocks.

—  —

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 Blocks are — and what they are not! (This is a free download).

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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).
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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 #262 — Another case of Mobitz I with Inferior MI.
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• ECG Blog #63 — Mobitz I with Junctional Escape Beats.
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• ECG Blog #80 — Reviews determination of the "culprit" artery and — application of the Mirror Test for recognition of acute Posterior MI.
• ECG Blog #246 — Reviews use of the "Mirror Test" to facilitate recognition of acute Posterior MI.
• ECG Blog #193 — Reviews the concept of "OMI" ( = Occlusion-based MI) — with an Audio Pearl that reviews the basics for predicting the "culprit" artery.
• ECG Blog #294 — Reviews a case to illustrate keep concepts regarding predicting the "culprit" artery — and appreciating when reperfusion occurs.
• ECG Blog #228 — Reviews the concept of "Silent" MI.
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• ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL.