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).
• 
  
• 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.
• 
  
• 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.

===================================

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.

===================================

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.
• 
  
• 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!
• 
  
• 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.

==================================

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

==================================

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).
• 
  
• 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).

=======================

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).
•  
• ECG Blog #164 — Which reviews step-by-step the diagnosis of a Mobitz I 2nd-degree AV block (with sequential laddergram illustration).
• 
  
• 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.
• 
  
• ECG Blog #63 — Mobitz I with Junctional Escape Beats.
•  
• 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.
• 
  
• ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL.

ECG Blog #471 — Two for One?

The ECG in Figure-1 was obtained from a man in his 60s — who presented with an acute, febrile pulmonary illness. He has been short of breath — but not having chest pain.

QUESTION:

• How would you interpret the ECG in Figure-1?

Figure-1: The initial ECG in today's case — obtained from a man in his 60s with dyspnea, but no chest pain. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

Interpretation of the ECG in Figure-1 is made more challenging by overlap of QRS complexes in multiple leads. That said — there appear to be 2 princpal elements to this rhythm: 

• i) The run of wide beats that begins this ECG (Seen for beats #1-thru-8 — and then for two 3-beat salvos that are seen later in the tracing); and, 
• ii) The lack of sinus P waves for the 2 short periods of narrower beats (ie, for beats #9-11; and 15-17).

PEARL: This is not an easy tracing to interpret. That said — When faced with a complex arrhythmia to interpret, in which there are a number of challenging elements — I find it helpful to: 

• i) Look for an underlying rhythm.
• ii) Begin with those elements that are easier to interpret.

I highlight these points in Figure-2:

• Instead of sinus P waves — Don't the regularly-occurring RED lines in Figure-2 suggest the "sawtooth" pattern of AFlutter (Atrial Flutter) as the underlying rhythm? 
• The rate of these RED lines is approximately 1 large box in duration — or close to 300/minute (which is perfectly consistent with the atrial rate of untreated AFlutter).
• The R-R interval for these 6 supraventricular beats (ie, Narrow QRS complexes #9,10,11 and #15,16,17) — is close to 2 large boxes in duration, which is perfectly consistent to AFlutter with 2:1 AV conduction as the underlying rhythm.

This leaves us to contemplate the etiology of the wide beats:

• As noted earlier — ECG #1 begins with a run of 8 wide beats (beats #1-thru-8 in Figure-2) — with two additional 3-beat runs (beats #9-11 and 15-17). Determining whether these wide beats represent ventricular beats vs supraventricular beats with aberrant conduction is the more difficult part of this tracing.

Figure-2: I've labeled flutter waves — here best seen in lead III.

Assessing the Wide Beats:

Overall — the wide beats appear to be fairly (but not completely) regular. This slight irregularity is best appreciated by looking at the R-R interval in lead II of Figure-3 between beats #12-13 vs between beats #13-14.

• The overall rate of the wide beats is a bit over 150/minute (ie, the R-R interval is less than 2 large boxes in duration).
• In contrast — I thought the narrow beats during AFlutter manifested a more consistently regular rate (as is common with 2:1 AFlutter).
• There are 2 post-ectopic pauses in Figure-3 (highlighted by the double YELLOW arrows). Post-ectopic pauses are a common feature following a run of VT (Ventricular Tachycardia).
• Doesn't the QRS complex of beat #9 in several leads (especially in leads II,III,aVF) look intermediate in morphology between the wide beats that precede it and narrow beats #10,11 that come after it? I therefore thought beat #9 was a fusion beat ("F" in Figure-3) — which if correct, would provide support that the wide beats in today's rhythm were ventricular.
• Finally — QRS morphology of the wide beats in Figure-3 strongly suggests a ventricular etiology because: i) Transition in the chest leads occurs much earlier than expected for Left Bundle Branch Block conduction (ie, the R wave is already all positive by lead V4 — whereas transition usually does not occur with LBBB until at least lead V5, if not V6); ii) LBBB conduction typically manifests a wider monophasic R wave in lead I than in leads II and III — and — LBBB conduction does not produce an all negative QRS in lead aVL (as we see here); — and, iii) The frontal plane axis of the wide beats in Figure-3 is vertical (ie, most positive in leads II,III,aVF compared to lead I ) — which results in a QRS morphology consistent with RVOT VT (Right Ventricular Outflow Track VT) — namely, LBBB-like morphology in the chest leads with an inferior frontal plane axis.

========================================

• NOTE: See ECG Blog #204 (for more on "typical" QRS morphology with LBBB & RBBB, including an ECG Video) — and ECG Blog #323 (for more on the appearance of idiopathic VT, including RVOT VT which is the most common form).

Figure-3: I've labeled post-ectopic pauses and a probable fusion beat.

BOTTOM Line: It's impossible to be 100% certain as to the etiology of the wide beats in today's tracing. That said:

• The underlying rhythm appears to be AFlutter with 2:1 AV conduction.
• The ECG features described above make it most likely that the runs of wide beats in today's rhythm represent NSVT (Non-Sustained Ventricular Tachycardia). We don't know how long the 1st run is (since the tracing begins with VT). After a brief pause — we then see two 3-beat salvos.
• Without more information — it's hard to know what optimal treatment should be. Both AFlutter and PVCs (including NSVT) are commonly seen with hypoxemia — and often resolve once the pulmonary problem and oxygen status are stabilized. Cardioversion is not indicated — since the runs of VT are not sustained. More information is needed.
• Final Thought: I generally look for a single explanation to most of the arrhythmias I encounter. That said — today's case provides an insightful example of ECG features that suggest the occurrence of both an underlying supraventricular rhythm ( = AFlutter) — and, a superimposed ventricular rhythm (ie, repetitive PVCs with a run of NSVT).

==================================

Acknowledgment: My appreciation for the anonymous donation of today's case and this tracing.

================================== 

==============================

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 #287 — Review of AFlutter ...
• 
  
• 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 — Blog #384 — 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 #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 — Another regular WCT rhythm ...
• 
  
• 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 #470 — This ECG Tells a Story

The ECG in Figure-1 was obtained from a previously healthy middle-aged man — who presented to the ED (Emergency Department) with new-onset CP (Chest Pain) that began ~1 hour earlier.

QUESTION:

The title I chose for today’s Blog post is, “This ECG tells a story”.

• What is “the Story” that this initial ECG tells? 

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

MY Thoughts on Today’s CASE:

Unfortunately, there is no long lead rhythm strip in Figure-1. That said — there appears to be a regular, wide-QRS rhythm, at a rate of ~80/minute.

• There appear to be some P waves — but these do not seem to be related to neighboring QRS complexes, as the PR interval continually changes (RED arrows in Figure-2). This suggests there is AV dissociation — which if truly present, suggests a ventricular etiology for the wide-QRS rhythm. 

Figure-2: I've labeled readily visible P waves with RED arrows.

Support that the underlying rhythm in Figure-2 is ventricular — is forthcoming from assessment of QRS morphology (See Figure-3). The following morphologic features are not consistent with any known form of conduction defect:

• The fragmented but all negative QRS complex in lead I.
• The wide and deep Q waves that are seen in each of the 6 chest leads.
• Slow initial depolarization in each of the chest leads (ie, the downslope of virtually all Q waves and QS complexes is “slow” and gradual — whereas depolarization of the initial portion of the QRS tends to be faster with supraventricular rhythms that travel over the specialized conduction system). 
• The predominantly negative and fragmented QRS in lead V6 (The QRS complex in left-sided lead V6 will almost always have more positivity than seen here when the rhythm is supraventricular).
• 
  
• PEARL #1: More than simply suggesting a ventricular etiology for the rhythm in Figure-3 — the wide and deep Q waves (or QS complexes) in 8/12 leads (slanted blue lines) — especially given the fragmentation that we see in several leads (especially in I,V5,V6) — strongly suggests "scar" that most probably is due to prior infarction.

PEARL #2: Despite the challenge of assessing a ventricular rhythm for underlying ischemia and/or infarction — there are primary ST-T wave changes that are seen in Figure-3 that suggest an ongoing acute event.

• Most notable among these “primary” ST-T wave changes in ECG #1 — include coved ST elevation that begins in lead V2 — and continues across the precordial leads until lead V6. Of note — this coved ST elevation is greatest in lateral chest leads V5 and V6 (BLUE arrows in Figure-3).
• To Emphasize: The shape and amount of ST elevation in the chest leads is so pronounced — as to clearly indicate a recent (and potentially ongoing) acute event until proven otherwise.
• Abnormal ST elevation is also seen in the high-lateral limb leads ( = leads I and aVL) — which together with the abnormal (and very large) Q waves and QS complexes in 8/12 leads — suggests that the reason for this ventricular rhythm is a recent and/or ongoing extensive antero-lateral STEMI.

Figure-3: I’ve labeled the abnormal Q waves (and QS complexes) — and the leads showing abnormal ST elevation in this ventricular rhythm.

================================

The CASE Continues:

• Troponin was positive. This supports the suggestion of ongoing acute infarction.
• The long lead II rhythm strip shown in Figure-4 was obtained.

QUESTIONS:

• What is the rhythm in Figure-4?
• Are we seeing AIVR (Accelerated IdioVentricular Rhythm) — that often appears as a short-lived and usually benign ventricular rhythm that may signal reperfusion in a patient with acute infarction? (See ECG Blog #321 and ECG Blog #108 — for more on AIVR).

Figure-4: Long lead II rhythm seen in today's patient.

ANSWER:

Easy to overlook when assessing the rhythm strip in Figure-4 from today's case — is the finding that although the QRS complex in this long lead II rhythm strip is wide — QRS morphology is very different than the QRS morphology that was seen previously in lead II (Go back and compare the previously positive QRS morphology in lead II of Figure-3 — with the now predominantly negative QRS in Figure-4). 

• This change that we see in QRS morphology in lead II — suggests that the site of the ventricular rhythm we are now looking at in Figure-4, has changed from what it was previously. This can occur, and in today's case — was not felt to represent a change in the overall ongoing rhythm, since the changing relationship between P waves and neighboring QRS complexes over the course of the next few hours (and as it turned out, ensuing days) on telemetry monitoring remained the same.
• Throughout this time period — the patient remained hemodynamically stable and surprisingly without symptoms!
• The patient refused cardiac catheterization. Instead — he felt well, and ultimately decided to go home a few days later. The patient left before a final ECG could be done — so we do not know what the rhythm was at the time the patient left the hospital.

What Then is the Rhythm in Figure-4?

I find the easiest way to assess rhythms such as the one in Figure-4 — is by labeling P waves. Doing so facilitates assessment of the relationship (if any) of P waves with neighboring QRS complexes. I have labeled P waves in Figure-5.

• RED arrows in Figure-5 highlight those P waves that we can readily identify.
• PINK arrows highlight where my calipers suggest on-time P waves are probably hiding (with subtle peaking or "extra bulging" in a number of T waves, thus supporting my suspicion of on-time sinus P waves below these arrows).
• Note that the PR interval in front of the 13 QRS complexes in Figure-5 is constantly changing, Thus we have a fairly regular wide-QRS (ventricular) rhythm at ~80-85/minute — and an independent, fairly regular underlying sinus rhythm, but with no relationship between on-time sinus P waves and neighboring QRS complexes (ie, there is complete AV dissociation).
• Technically — the diagnosis of complete (3rd-degree) AV block is difficult to make in the absence of a ventricular escape rhythm below ~50-55/minute (because of the difficulty demonstrating at ventricular rates that are over 55-60/minute that all P waves have adequate opportunity to conduct — yet still fail to do so). That said — today's patient maintained this same rhythm over time — so this rhythm was thought to represent 3rd-Degree AV Block.
• PEARL #3: Another point in support of this rhythm being complete AV block — is that the atrial rhythm is faster than the ventricular rhythm. Under normal circumstances — this should enable the more rapidly occurring sinus P waves at some point to regain control of the rhythm IF there is not complete AV block. Instead, none of the sinus P waves are able to conduct to the ventricles.

Figure-5: I've labeled with colored arrows what appears to represent an underlying sinus rhythm for the tracing in Figure-4.

Laddergram of Figure-5:

As opposed to AIVR, in which there is an accelerated ventricular rhythm with either no P waves or with retrograde P waves — the rhythm in Figure-5 appears to be complete AV block. 

• I represent this in the laddergam shown in Figure-6. The Atrial Tier shows fairly regular sinus P waves (slight ventriculophasic sinus arrhythmia) — and a fairly regular accelerated ventricular "escape" rhythm — but without any of the on-time sinus P waves being able to conduct to the ventricles as a result of complete AV block (double dotted lines in the AV Nodal Tier depicting the barrier preventing conduction of any sinus impulses to the ventricles).

Figure-6: Complete AV dissociation. The double dotted line suggests this is the result of complete AV block.

================================

CASE Conclusion: The Story Told in Today's Case ...

Putting the "story" together in today's case:

• In Figure-7 — are 2 additional 12-lead ECGs that were obtained during the course of this patient's hospitalization. Although difficult to assess the rhythm in these 2 tracings without the benefit of any accompanying long lead rhythm strips — intermittent P waves with variable PR intervals appear to be present in both tracings, suggesting persistence of the same rhythm that we saw in Figure-6.
• If we review the serial ECGs in today's case (that I've put together in Figure-7) — there is clear evolution of an extensive antero-lateral STEMI (ie, increased ST elevation, especially in leads V4,V5,V6 in ECG #2 — followed by a fall in ST elevation with more pronounced T wave inversion, especially in the inferior leads of ECG #3). 
• PEARL #4: Today's case therefore provides an excellent example of how serial ST-T wave morphology changes in ventricular beats may at times provide insight to the evolutionary changes of acute infarction. The reduction in ST elevation with deepening T wave inversion in ECG #3 suggests there has been some amount of reperfusion.

PEARL #5: Distinction between infarction-related AIVR (which is usually a transient and benign ventricular rhythm that often occurs in association with acute MI) — vs — development of complete AV block (as occurred in today's case) — has important clinical implications:

• In most instances — No treatment is needed for AIVR.
• In contrast — emergency (and/or longterm) pacing may be needed when complete AV block is the result of acute infarction. This is especially true when AV block arises as the result of an extensive anterior STEMI, as in today's case (as opposed to AV block that occurs in association with acute inferior MI, which is much more likely to be transient — and much less likely to need pacing).

Optimal Management of today's CASE — would therefore include prompt cardiac catheterization with PCI as the best chance for resolving the 3rd-degree block. 

• If 3rd-degree AV block persists despite PCI (especially if associated with hemodynamic instability) — then emergency pacing will be needed, at least temporarily (ie, Guidelines suggest not to implant a permanent pacemaker for at least a few days following PCI — in the event of spontaneous recovery of AV conduction).
• 
  
• The above said — Today's patient had other ideas. He remained remarkably stable despite the above conduction disorder. He ultimately decided to leave the hospital at some point after ECG #3, after which he was lost to follow-up.
• What then is "the Story?" — The "story" that I quickly derived on seeing today's initial ECG — is that the regular wide-QRS rhythm in Figure-1, with apparent AV dissociation — represents complete AV block, most likely resulting from recent (and/or ongoing) extensive antero-lateral STEMI.

Figure-7: Serial ECGs in today's case. 

================================

Potential Final Outcomes: Today's patient amazingly became asymptomatic after a day or so in the hospital. He refused cardiac cath and PCI — and — since he was feeling well, decided to go home.

• It's obvious from the serial ECGs shown in Figure-7 — that significant myocardium was lost from extensive infarction. That said, despite complete AV block — the normal ventricular rate (of ~80/minute) provided by this patient's accelerated ventricular "escape" rhythm was apparently maintaining sufficient cardiac output to render him "asymptomatic".
• In the Best Case Scenario — this patient's 3rd-degree AV block will spontaneously resolve. In this case, despite significant functional loss from his extensive infarction — he may be able to continue sufficient daily activity acceptable for his lifestyle. We wish for this best case scenario outcome!
• In a Less Optimal Case Scenario — this patient's 3rd-degree AV block might not only become permanent, but the ventricular "escape" rhythm will probably slow down at some point to the the usual 20-40/minute idioventricular escape rate. In this less optimal case scenario — the patient will hopefully remain alive long enough to return for permanent pacing.

==================================

Acknowledgment: My appreciation to Fardeen Baray a (from Kabul, Afghanistan) for the case and this tracing.

• Special THANKS to Dr. Willy Frick — for his Cardiology insights on this case.

==================================

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

Figure-8: 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!" ).

==========================  

• For more on AIVR — See ECG Blog #108 — and ECG Blog #321 —